自咬症水貂行为规律及抗氧化系统研究
|
摘要
水貂自咬症是水貂无意识的一种自我损伤行为,但是并不清楚这一种异常行为的生物学基础。本研究用当年繁殖和断奶后的育成水貂,通过自咬症水貂和临床健康水貂行为学的比较研究;机体抗氧化酶活性和甲基汞与总汞的测定;钙离子通道抑制剂对自咬行为的影响研究;抗氧化微营养维生素E以及亚硒酸钠对水貂自咬症发生的影响研究和水貂神经系统病理组织学研究,探讨导致水貂自咬症的原因。本项目通过以上研究取得以下成果:
1水貂自咬行为规律及管理应激对水貂行为的影响
随机选择当年断奶的60只自咬症水貂和60只临床健康水貂,公母各半,每个组3个重复,每个重复20只水貂,公母各半,每天观察水貂自咬行为发生的时间规律;通过转群以及连续3 d的模拟捕捉和注射,观察管理应激对自咬症水貂和临床健康水貂自咬频率和行为呆板症发生率的影响。结果表明,水貂自咬行为呈现间歇发作,发病时间主要集中在夜间和投喂食物前后,每年的7月和9月是自咬症的发病高峰期,自咬频率在该时期也最高。自咬症水貂和临床健康水貂均有行为呆板症发生,发生率分别为19.44%和11.67%;转群、连续3天的捕捉和注射会刺激自咬症水貂,水貂自咬频率显著升高,但随后的6 d和9 d呈现线性下降。管理应激同样也提高了健康水貂和自咬症水貂行为呆板症的发生率,但第6 d和第9 d也呈现下降的趋势。研究结果表明,水貂自咬行为是一种间歇性发作的神经行为疾病;行为呆板症在健康水貂和自咬症水貂群体中都有发生;转群、捕捉和注射等管理应激会刺激水貂自咬行为和行为呆板症的发生。
2自咬症水貂机体抗氧化系统与汞残留的相关性研究
随机选择健康和自咬症水貂雌雄各10只,心脏采血,用血液自动分析仪测定血液生理生化指标。随机选择自咬症和临床健康水貂各20只,空气心脏注射致死,快速去皮,采集肝脏、肾脏、大脑和肌肉样品,用于机体抗氧化酶活性、总汞和甲基汞等指标的测定。研究结果表明,自咬症水貂和临床健康水貂的红细胞数、血红蛋白含量、红细胞平均容积、血小板数等指标没有差异,但是白细胞数均极显著地高于临床健康水貂(p<0.01)。自咬症水貂肝脏和脑中的GSH水平明显低于健康水貂(p<0.01)。其中脑中的GSH水平只有正常水貂的76%。自咬症水貂体肝脏和大脑中VE水平分别比正常水貂低22.5%和21.1%。
自咬症水貂两器官中总SOD和Cu/Zn-SOD,以及肝脏中的Mn-SOD显著或极显著地高于对照组(p <0.05或p <0.01)。自咬症水貂肝脏和大脑中的CAT酶活性均极显著地降低(p <0.01),其中肝脏降低34% ,大脑中降低21%。SBB水貂机体内GPx活性也有降低,但只有大脑中明显低于正常水貂。自咬症水貂大脑和肝脏中MDA分别比健康水貂高51%和22%。自咬症水貂大脑和肝脏中蛋白质羧基化程度明显高于健康组水貂。与健康组相比,自咬症水貂大脑和肝脏中PC分别高30 %和18.5 %。自咬症水貂大脑Ca2+-ATPase活性显著低于健康水貂,NOS活性也显著低于临床健康水貂组。
自咬症水貂机体内甲基汞和总汞蓄积均显著高于健康组,其中自咬症水貂肝脏和大脑甲基汞分别比对照组高20%和48.8%,总汞分别比对照组高16%和44.8%。但自咬症水貂肾脏甲基汞和总汞含量与对照组没有显著差异。自咬症水貂甲基汞及总汞与GSH及MDA之间的相关性同健康组不同。在健康组,只有大脑中的MeHg及THg浓度与GSH水平成负相关。而肝脏、肾脏和大脑中氧化应激生物标记物MDA水平与MeHg及THg浓度之间均没有相关性。在自咬症水貂组,肝脏和大脑中的甲基汞浓度,以及大脑中总汞浓度均与同一组织中的GSH水平呈明显的负相关(p<0.01)。被测三器官中的MDA与MeHg及总汞均呈正相关。
3 VE亚硒酸钠复合剂和尼莫地平对水貂自咬行为的影响研究
试验选择72只标准色自咬症水貂,雌雄各半,随机分为3个组,每个组3个重复,每个重复8只自咬症水貂。试验分为3个处理,分别为对照组、尼莫地平组、维生素E+亚硒酸钠+尼莫地平组。对照组为基础日粮组;尼莫地平组:在基础日粮中添加25mg/kg的尼莫地平。每只水貂的饲料投喂量为200g左右/d。每只自咬症水貂每天尼莫地平的摄入量为5mg左右;维生素E+亚硒酸钠+尼莫地平组:在日粮中添加50ppm维生素E、5ppm亚硒酸钠和25ppm尼莫地平。研究钙离子通道抑制剂和抗氧化维生素对水貂自咬症的影响。试验结果表明,在日粮中添加钙离子通道抑制剂后,水貂自咬症的发生逐渐下降,但是到12d以后,这种逐渐消失,自咬症发生频率又有一定的升高,但在试验的21d中,自咬频率都低于对照组;尼莫地平和维生素E+亚硒酸钠复合剂共同作用显著地降低了自咬症水貂自咬发生频率,这种变化在投药的第9d基本保持较为稳定,而且自咬症的发生频率没有再次上升。
4 VE和亚硒酸钠对水貂自咬症发病率及机体抗氧化酶水平和汞残留的影响
选择当年断奶的1920只没有自咬行为的仔貂,随机分为2个组,每个组4个重复,每个重复240只水貂。试验组在养殖场常规日粮基础上额外添加50ppm维生素E和5ppm亚硒酸钠,研究其对自咬症的发生率的影响;随机选择实验组和对照组水貂各32只,空气注射法处死水貂,采肝脏、大脑和肾脏样品,测定GSH、VE和抗氧化酶活性和甲基汞残留。实验结果表明,维生素E和亚硒酸钠添加组均极显著地显著降低了水貂自咬症的发生率(p<0.01)。在水貂日粮中添加维生素E和亚硒酸钠复合剂极显著地提高了水貂肝脏维生素E的水平(p<0.01),实验组肝脏和大脑中的GSH水平都显著高于对照组(p<0.05)。维生素E+亚硒酸钠复合剂能够极显著地提高水貂大脑和肝脏组织中的GPx水平(p<0.01);同时也极显著提高了水貂肝脏CAT的活性(p<0.01),但对大脑的CAT活性影响不大。
实验组肝脏和大脑中CuZn-SOD活性显著或者极显著地低于对照组(p<0.05 or 0.01),而T-SOD、Mn-SOD活性无显著差异。维生素E+亚硒酸钠复合剂能够显著降低水貂大脑和肝脏中甲基汞的含量(p<0.05),但是对肾脏中甲基汞的含量无显著影响。维生素E+亚硒酸钠复合剂极显著降低了水貂肝脏和大脑MDA的水平(p<0.01)。5自咬症水貂神经系统病理组织学研究
试验采集20只临床健康水貂和20只自咬症水貂的大脑、小脑、延脑和脊髓等神经系统组织,用体积分数4%多聚甲醛固定后经选样、脱水、透明、石蜡包埋、切片和H.E染色,在200～400倍光学显微镜下进行观察并对比病理变化。显微观察结果表明,与临床健康水貂相比,自咬症水貂大脑中普遍存在神经细胞肿胀、溶解以及神经细胞卫星现象;部分神经锥体细胞固缩变形,细胞膜周边出现空泡化,神经纤维溶解消失,神经细胞核固缩浓染;部分自咬症水貂大脑的髓质出现空泡化,神经胶质细胞膜内侧浓染;小脑中的浦肯野氏细胞普遍存在肿胀、融解以及神经髓鞘溶解现象。延脑神经细胞肿胀,大胶质细胞膜溶解消失,神经椎体细胞周边出现严重的卫星现象;脊髓神经细胞明显肿胀,细胞膜消失,神经细胞核固化萎缩。病理组织学研究结果表明,水貂自咬症与神经细胞膜结构损伤、神经传导细胞以及神经髓鞘的病变有关。
Self-biting behavior was unconscious self-injurious behavior in mink,but little was known about the biological basis of this disorder. All minks in this study were young mink weaned present year in Jinzhou mink farm in Dalian. The subject of this research was to compare the behavior of self-biting mink and health mink, to test anti-oxidative enzyme activity, methyl mercury (MeHg) and total mercury (THg) , to determine the effect of Ca2+ channel inhibitor on self-biting behavior, to research on the effect of VE+Na2SeO3 on self-biting behavior and oxidative enzyme activity. The nervous system pathological changes in mink with self-injurious behavior also were investigated in this study. The research result saw as below:
1 Rules of self-biting behavior and the effect of management stress on behavior in farmed mink.
60 self-biting minks and 60 clinical health minks (half male and half female) were choose from weaned mink in current year, each group 20 minks(half male and half female); investigated the self-biting behavior regular. Moved mink house, and caught and injected within 3 day to research the effect of managing stress on self-biting frequency and stereotypical behavior in mink. The result shown that self-biting behavior was intermittent occurrences; self-biting time was centered in night and the time before feeding. July and September is the peak of self-biting behavior, and self-biting frequency also reached the peak data. Both self-biting group and clinical health group have stereotypical behavior. The rate of incidence of stereotypical behavior was 19.44% and 11.67% respectively. Moved mink house, and catching and injecting within 3 day increased the self-biting frequency significantly, but it shown the down trend in next 6 and 9 day. This managing stress also increased stereotypical behavior rate in health and self-biting mink, it has same trend with self-biting frequency. Self-biting behavior is intermittent occurrence neurologic behavioral disease; stereotypical behavior happened both in self-biting mink and health mink. Moving house, catching and injecting stimulated the incidence of self-biting and stereotypical behavior.
2 Anti-oxidative system and correlation with Hg residue of self-biting mink
10 male and female minks were selected randomly from self-biting and health mink respectively, taken blood by cardiac puncture, to test hematological and biochemical Indexes of self-biting and health mink. 20 health and self-biting minks were selected randomly, heart-air-injection to death and take liver, kidney, brain and muscle samples to test the anti-oxidative enzyme activity, THg and MeHg. The results shown that, RBC, Hgb, MCV, MCH and BPC had no difference between self-biting mink and health mink. But WBC of self-biting mink was higher significantly than health mink(p<0.01). GSH level in self-biting mink was lower than health mink( p<0.01). The content of GSH was only 76% compare with normal mink. VE level in liver and brain of self-biting mink also was 22.5% and 21.1% lower than health mink. SBB minks had higher total superoxide dismutase (SOD), Cu/Zn-SOD and Mn-SOD activities in both tissues (p <0.05 or p <0.01). Catalase (CAT) activities in liver and brain tissues of SBB minks were markedly lower than those of normal group (p <0.01). GPx activities also lower than normal mink, but only have significant different in brain. SBB minks produced more MDA with 51% increase in brain (p <0.01) and 22% increase in liver (p <0.01) compared to normal minks. Similarly, the hepatic and cerebral PC in SBB minks were 18.5% (p <0.01) and 30% higher (p<0.001), respectively. Ca2+-ATPase and NOS activities in the brain of SBB minks were lower than health mink (p <0.01). SIB minks accumulated more cerebral MeHg and hepatic THg compared to the normal minks (p <0.05 or p <0.01) with 48.8% increase in brain and 20% increase in liver of MeHg, 16% increase in liver and 44.8% increase in brain of THg. But there were no significant differences in kidney between the two groups. The correlation between MeHg or THg accumulation and GSH or MDA levels in SIB group was not consistent with that in normal group. In normal group, only cerebral GSH had negatively correlation with MeHg or THg concentrations. While in SIB group, both cerebral and hepatic GSH level had negative effect on MeHg accumulation, and a significantly positive correlation between MDA and MeHg or THg was found in all of the three tissues.
3 The effect of VE+Na2SeO3 and Nimodipine on self-biting behavior in mink
72 standard color minks with self-biting behavior were selected, half male and half female, divide into 3 group, 3 repeats in each group and 8 self-biting minks in each repeat. 3 treatments were control, Nimodipine and Nimodipine+VE+Na2SeO3 respectively. In Nimodipine group, 25ppm nimodipine was add in mink feed. The feed supply was 200g each mink each day. Nimodipine intake was 5mg each mink each day. 50ppm VE, 5ppm Na2SeO3 and 25ppm nimodipine was added in mink feed in Nimodipine+VE+Na2SeO3 group. The study of this research was to determine the effect of Ca2+ channel inhibitor and Vitamin E and Na2SeO3 on the self-biting behavior. The result shown that, self-biting frequency decreased remarkable in the beginning, but this effect reduced day by day after 12 d in Nimodipine group, the self-biting frequency increased again. But the self-biting frequency lower than control group in experiment period. Nimodipine+VE+Na2SeO3 decreased self-biting frequency significantly after 9 d of treatment, this effect continued in all experiment period.
4 The effect of VE+Na2SeO3 on accidence rate of self-biting and anti-oxidative enzyme activity and Hg residue in mink.
1920 weaned minks were selected randomly and divided into 2 groups, each group has 4 repeats, 240 minks in each repeats. 50ppm VE and Na2SeO3 add in feed of treatment group to research the effect on accident rate of self-biting. Selected 32 minks in every group before take fur in winter, heart-air-injection to death and taken liver, kidney and brain samples to test GSH, VE level, anti-oxidative enzyme activity and MeHg residue in tissues. Experiment result shown that, VE+Na2SeO3 group decreased the self-biting accident rate of mink significantly(p<0.01). VE level increased in liver in treatment group(p<0.01), GSH level in liver and brain also higher than control group(p<0.05). VE +Na2SeO3 improved GPx activities in brain and liver(p<0.01), and CAT in liver also increased in treatment group(p<0.01), but have no effect on CAT activity in brain tissue. CuZn-SOD activities in liver and brain were lower than control group( p<0.05 or 0.01),but no effect on T-SOD、Mn-SOD. VE+Na2SeO3 decreased MeHg level in brain and liver significantly (p<0.05), but have no effect on HeHg level in kidney. VE+Na2SeO3 treatment decreased MDA level in liver and brain significantly (p<0.01).
5 Histopathological studies on nervous system in self-biting behavior mink
The cerebrum, cerebellum, medulla oblongata and medulla marrow from each of 20 healthy minks and 20 self-injurious minks were collected in current study. All samples were fixed in 4% paraformaldehyde, followed by dewatering, hyalining, paraffin embedding, slicing and hematoxylin eosin staining. All sections were observed at 200- 400 times light microscope. Compared with clinical health mink, histopathological changes were found in nervous system of minks with self-injurious behavior. Swelling, lysing and microsatellite phenomenon of nerve cells were observed in the cerebrum. Many nuclei in nerve cells became pyknotic (shrunken and dark). Vacuolizations were observed in cerebrum of some minks with self-injurious behavior. Intracellular membrane of neuroglia cell was deeply stained. Swollen and lysed Purkinje cells were investigated in cerebellum, and some of the myelin sheaths were lysed in this region. Neurocyte swelling, membrane ablation of macroglia and serious microsatellite phenomenon were observed in medulla oblongata of SIB mink. Nerve cells pyknotic and membrane lysed also found in spinal marrow. Self-injurious behavior of minks has correlation with pathological changes of membrane of nerve cell and nerve myelin sheath.
1水貂自咬行为规律及管理应激对水貂行为的影响
随机选择当年断奶的60只自咬症水貂和60只临床健康水貂,公母各半,每个组3个重复,每个重复20只水貂,公母各半,每天观察水貂自咬行为发生的时间规律;通过转群以及连续3 d的模拟捕捉和注射,观察管理应激对自咬症水貂和临床健康水貂自咬频率和行为呆板症发生率的影响。结果表明,水貂自咬行为呈现间歇发作,发病时间主要集中在夜间和投喂食物前后,每年的7月和9月是自咬症的发病高峰期,自咬频率在该时期也最高。自咬症水貂和临床健康水貂均有行为呆板症发生,发生率分别为19.44%和11.67%;转群、连续3天的捕捉和注射会刺激自咬症水貂,水貂自咬频率显著升高,但随后的6 d和9 d呈现线性下降。管理应激同样也提高了健康水貂和自咬症水貂行为呆板症的发生率,但第6 d和第9 d也呈现下降的趋势。研究结果表明,水貂自咬行为是一种间歇性发作的神经行为疾病;行为呆板症在健康水貂和自咬症水貂群体中都有发生;转群、捕捉和注射等管理应激会刺激水貂自咬行为和行为呆板症的发生。
2自咬症水貂机体抗氧化系统与汞残留的相关性研究
随机选择健康和自咬症水貂雌雄各10只,心脏采血,用血液自动分析仪测定血液生理生化指标。随机选择自咬症和临床健康水貂各20只,空气心脏注射致死,快速去皮,采集肝脏、肾脏、大脑和肌肉样品,用于机体抗氧化酶活性、总汞和甲基汞等指标的测定。研究结果表明,自咬症水貂和临床健康水貂的红细胞数、血红蛋白含量、红细胞平均容积、血小板数等指标没有差异,但是白细胞数均极显著地高于临床健康水貂(p<0.01)。自咬症水貂肝脏和脑中的GSH水平明显低于健康水貂(p<0.01)。其中脑中的GSH水平只有正常水貂的76%。自咬症水貂体肝脏和大脑中VE水平分别比正常水貂低22.5%和21.1%。
自咬症水貂两器官中总SOD和Cu/Zn-SOD,以及肝脏中的Mn-SOD显著或极显著地高于对照组(p <0.05或p <0.01)。自咬症水貂肝脏和大脑中的CAT酶活性均极显著地降低(p <0.01),其中肝脏降低34% ,大脑中降低21%。SBB水貂机体内GPx活性也有降低,但只有大脑中明显低于正常水貂。自咬症水貂大脑和肝脏中MDA分别比健康水貂高51%和22%。自咬症水貂大脑和肝脏中蛋白质羧基化程度明显高于健康组水貂。与健康组相比,自咬症水貂大脑和肝脏中PC分别高30 %和18.5 %。自咬症水貂大脑Ca2+-ATPase活性显著低于健康水貂,NOS活性也显著低于临床健康水貂组。
自咬症水貂机体内甲基汞和总汞蓄积均显著高于健康组,其中自咬症水貂肝脏和大脑甲基汞分别比对照组高20%和48.8%,总汞分别比对照组高16%和44.8%。但自咬症水貂肾脏甲基汞和总汞含量与对照组没有显著差异。自咬症水貂甲基汞及总汞与GSH及MDA之间的相关性同健康组不同。在健康组,只有大脑中的MeHg及THg浓度与GSH水平成负相关。而肝脏、肾脏和大脑中氧化应激生物标记物MDA水平与MeHg及THg浓度之间均没有相关性。在自咬症水貂组,肝脏和大脑中的甲基汞浓度,以及大脑中总汞浓度均与同一组织中的GSH水平呈明显的负相关(p<0.01)。被测三器官中的MDA与MeHg及总汞均呈正相关。
3 VE亚硒酸钠复合剂和尼莫地平对水貂自咬行为的影响研究
试验选择72只标准色自咬症水貂,雌雄各半,随机分为3个组,每个组3个重复,每个重复8只自咬症水貂。试验分为3个处理,分别为对照组、尼莫地平组、维生素E+亚硒酸钠+尼莫地平组。对照组为基础日粮组;尼莫地平组:在基础日粮中添加25mg/kg的尼莫地平。每只水貂的饲料投喂量为200g左右/d。每只自咬症水貂每天尼莫地平的摄入量为5mg左右;维生素E+亚硒酸钠+尼莫地平组:在日粮中添加50ppm维生素E、5ppm亚硒酸钠和25ppm尼莫地平。研究钙离子通道抑制剂和抗氧化维生素对水貂自咬症的影响。试验结果表明,在日粮中添加钙离子通道抑制剂后,水貂自咬症的发生逐渐下降,但是到12d以后,这种逐渐消失,自咬症发生频率又有一定的升高,但在试验的21d中,自咬频率都低于对照组;尼莫地平和维生素E+亚硒酸钠复合剂共同作用显著地降低了自咬症水貂自咬发生频率,这种变化在投药的第9d基本保持较为稳定,而且自咬症的发生频率没有再次上升。
4 VE和亚硒酸钠对水貂自咬症发病率及机体抗氧化酶水平和汞残留的影响
选择当年断奶的1920只没有自咬行为的仔貂,随机分为2个组,每个组4个重复,每个重复240只水貂。试验组在养殖场常规日粮基础上额外添加50ppm维生素E和5ppm亚硒酸钠,研究其对自咬症的发生率的影响;随机选择实验组和对照组水貂各32只,空气注射法处死水貂,采肝脏、大脑和肾脏样品,测定GSH、VE和抗氧化酶活性和甲基汞残留。实验结果表明,维生素E和亚硒酸钠添加组均极显著地显著降低了水貂自咬症的发生率(p<0.01)。在水貂日粮中添加维生素E和亚硒酸钠复合剂极显著地提高了水貂肝脏维生素E的水平(p<0.01),实验组肝脏和大脑中的GSH水平都显著高于对照组(p<0.05)。维生素E+亚硒酸钠复合剂能够极显著地提高水貂大脑和肝脏组织中的GPx水平(p<0.01);同时也极显著提高了水貂肝脏CAT的活性(p<0.01),但对大脑的CAT活性影响不大。
实验组肝脏和大脑中CuZn-SOD活性显著或者极显著地低于对照组(p<0.05 or 0.01),而T-SOD、Mn-SOD活性无显著差异。维生素E+亚硒酸钠复合剂能够显著降低水貂大脑和肝脏中甲基汞的含量(p<0.05),但是对肾脏中甲基汞的含量无显著影响。维生素E+亚硒酸钠复合剂极显著降低了水貂肝脏和大脑MDA的水平(p<0.01)。5自咬症水貂神经系统病理组织学研究
试验采集20只临床健康水貂和20只自咬症水貂的大脑、小脑、延脑和脊髓等神经系统组织,用体积分数4%多聚甲醛固定后经选样、脱水、透明、石蜡包埋、切片和H.E染色,在200～400倍光学显微镜下进行观察并对比病理变化。显微观察结果表明,与临床健康水貂相比,自咬症水貂大脑中普遍存在神经细胞肿胀、溶解以及神经细胞卫星现象;部分神经锥体细胞固缩变形,细胞膜周边出现空泡化,神经纤维溶解消失,神经细胞核固缩浓染;部分自咬症水貂大脑的髓质出现空泡化,神经胶质细胞膜内侧浓染;小脑中的浦肯野氏细胞普遍存在肿胀、融解以及神经髓鞘溶解现象。延脑神经细胞肿胀,大胶质细胞膜溶解消失,神经椎体细胞周边出现严重的卫星现象;脊髓神经细胞明显肿胀,细胞膜消失,神经细胞核固化萎缩。病理组织学研究结果表明,水貂自咬症与神经细胞膜结构损伤、神经传导细胞以及神经髓鞘的病变有关。
Self-biting behavior was unconscious self-injurious behavior in mink,but little was known about the biological basis of this disorder. All minks in this study were young mink weaned present year in Jinzhou mink farm in Dalian. The subject of this research was to compare the behavior of self-biting mink and health mink, to test anti-oxidative enzyme activity, methyl mercury (MeHg) and total mercury (THg) , to determine the effect of Ca2+ channel inhibitor on self-biting behavior, to research on the effect of VE+Na2SeO3 on self-biting behavior and oxidative enzyme activity. The nervous system pathological changes in mink with self-injurious behavior also were investigated in this study. The research result saw as below:
1 Rules of self-biting behavior and the effect of management stress on behavior in farmed mink.
60 self-biting minks and 60 clinical health minks (half male and half female) were choose from weaned mink in current year, each group 20 minks(half male and half female); investigated the self-biting behavior regular. Moved mink house, and caught and injected within 3 day to research the effect of managing stress on self-biting frequency and stereotypical behavior in mink. The result shown that self-biting behavior was intermittent occurrences; self-biting time was centered in night and the time before feeding. July and September is the peak of self-biting behavior, and self-biting frequency also reached the peak data. Both self-biting group and clinical health group have stereotypical behavior. The rate of incidence of stereotypical behavior was 19.44% and 11.67% respectively. Moved mink house, and catching and injecting within 3 day increased the self-biting frequency significantly, but it shown the down trend in next 6 and 9 day. This managing stress also increased stereotypical behavior rate in health and self-biting mink, it has same trend with self-biting frequency. Self-biting behavior is intermittent occurrence neurologic behavioral disease; stereotypical behavior happened both in self-biting mink and health mink. Moving house, catching and injecting stimulated the incidence of self-biting and stereotypical behavior.
2 Anti-oxidative system and correlation with Hg residue of self-biting mink
10 male and female minks were selected randomly from self-biting and health mink respectively, taken blood by cardiac puncture, to test hematological and biochemical Indexes of self-biting and health mink. 20 health and self-biting minks were selected randomly, heart-air-injection to death and take liver, kidney, brain and muscle samples to test the anti-oxidative enzyme activity, THg and MeHg. The results shown that, RBC, Hgb, MCV, MCH and BPC had no difference between self-biting mink and health mink. But WBC of self-biting mink was higher significantly than health mink(p<0.01). GSH level in self-biting mink was lower than health mink( p<0.01). The content of GSH was only 76% compare with normal mink. VE level in liver and brain of self-biting mink also was 22.5% and 21.1% lower than health mink. SBB minks had higher total superoxide dismutase (SOD), Cu/Zn-SOD and Mn-SOD activities in both tissues (p <0.05 or p <0.01). Catalase (CAT) activities in liver and brain tissues of SBB minks were markedly lower than those of normal group (p <0.01). GPx activities also lower than normal mink, but only have significant different in brain. SBB minks produced more MDA with 51% increase in brain (p <0.01) and 22% increase in liver (p <0.01) compared to normal minks. Similarly, the hepatic and cerebral PC in SBB minks were 18.5% (p <0.01) and 30% higher (p<0.001), respectively. Ca2+-ATPase and NOS activities in the brain of SBB minks were lower than health mink (p <0.01). SIB minks accumulated more cerebral MeHg and hepatic THg compared to the normal minks (p <0.05 or p <0.01) with 48.8% increase in brain and 20% increase in liver of MeHg, 16% increase in liver and 44.8% increase in brain of THg. But there were no significant differences in kidney between the two groups. The correlation between MeHg or THg accumulation and GSH or MDA levels in SIB group was not consistent with that in normal group. In normal group, only cerebral GSH had negatively correlation with MeHg or THg concentrations. While in SIB group, both cerebral and hepatic GSH level had negative effect on MeHg accumulation, and a significantly positive correlation between MDA and MeHg or THg was found in all of the three tissues.
3 The effect of VE+Na2SeO3 and Nimodipine on self-biting behavior in mink
72 standard color minks with self-biting behavior were selected, half male and half female, divide into 3 group, 3 repeats in each group and 8 self-biting minks in each repeat. 3 treatments were control, Nimodipine and Nimodipine+VE+Na2SeO3 respectively. In Nimodipine group, 25ppm nimodipine was add in mink feed. The feed supply was 200g each mink each day. Nimodipine intake was 5mg each mink each day. 50ppm VE, 5ppm Na2SeO3 and 25ppm nimodipine was added in mink feed in Nimodipine+VE+Na2SeO3 group. The study of this research was to determine the effect of Ca2+ channel inhibitor and Vitamin E and Na2SeO3 on the self-biting behavior. The result shown that, self-biting frequency decreased remarkable in the beginning, but this effect reduced day by day after 12 d in Nimodipine group, the self-biting frequency increased again. But the self-biting frequency lower than control group in experiment period. Nimodipine+VE+Na2SeO3 decreased self-biting frequency significantly after 9 d of treatment, this effect continued in all experiment period.
4 The effect of VE+Na2SeO3 on accidence rate of self-biting and anti-oxidative enzyme activity and Hg residue in mink.
1920 weaned minks were selected randomly and divided into 2 groups, each group has 4 repeats, 240 minks in each repeats. 50ppm VE and Na2SeO3 add in feed of treatment group to research the effect on accident rate of self-biting. Selected 32 minks in every group before take fur in winter, heart-air-injection to death and taken liver, kidney and brain samples to test GSH, VE level, anti-oxidative enzyme activity and MeHg residue in tissues. Experiment result shown that, VE+Na2SeO3 group decreased the self-biting accident rate of mink significantly(p<0.01). VE level increased in liver in treatment group(p<0.01), GSH level in liver and brain also higher than control group(p<0.05). VE +Na2SeO3 improved GPx activities in brain and liver(p<0.01), and CAT in liver also increased in treatment group(p<0.01), but have no effect on CAT activity in brain tissue. CuZn-SOD activities in liver and brain were lower than control group( p<0.05 or 0.01),but no effect on T-SOD、Mn-SOD. VE+Na2SeO3 decreased MeHg level in brain and liver significantly (p<0.05), but have no effect on HeHg level in kidney. VE+Na2SeO3 treatment decreased MDA level in liver and brain significantly (p<0.01).
5 Histopathological studies on nervous system in self-biting behavior mink
The cerebrum, cerebellum, medulla oblongata and medulla marrow from each of 20 healthy minks and 20 self-injurious minks were collected in current study. All samples were fixed in 4% paraformaldehyde, followed by dewatering, hyalining, paraffin embedding, slicing and hematoxylin eosin staining. All sections were observed at 200- 400 times light microscope. Compared with clinical health mink, histopathological changes were found in nervous system of minks with self-injurious behavior. Swelling, lysing and microsatellite phenomenon of nerve cells were observed in the cerebrum. Many nuclei in nerve cells became pyknotic (shrunken and dark). Vacuolizations were observed in cerebrum of some minks with self-injurious behavior. Intracellular membrane of neuroglia cell was deeply stained. Swollen and lysed Purkinje cells were investigated in cerebellum, and some of the myelin sheaths were lysed in this region. Neurocyte swelling, membrane ablation of macroglia and serious microsatellite phenomenon were observed in medulla oblongata of SIB mink. Nerve cells pyknotic and membrane lysed also found in spinal marrow. Self-injurious behavior of minks has correlation with pathological changes of membrane of nerve cell and nerve myelin sheath.
引文
崔剑,李兆龙,洪啸吟.2000.自由基生物抗氧化与疾病.清华大学学报:自然科学版,40(6):9
董为伟.2002.神经保护的基础与临床.北京:科学出版社:14-21
高宏伟,陈维岩,马振凯.1995.水貂自咬症研究概况.毛皮动物饲养,3:41-43
高宏伟,陈维岩.1994.自咬症水貂脑、肝、肾和毛中汞残留量的分析.毛皮动物饲养, 2:1-3
高颖,许彩民,杨洋.1998.氧化诱导K652细胞凋亡机制的初步探讨.中国生物化学与分子生物学学报,14(3):295-299
胡蓉玲,张淑珍.2004.蓝狐自咬症的诊治.中国动物保健,10:29-30
江勇. 1998.汞对内耳及神经系统的毒性作用.黑龙江畜牧兽医, 2:161-163
井明艳,赵树盛,付亮剑. 2006.硒的生化特性与谷胱甘肽系统.饲料工业,4:8-11
李长胜.1998.狐貉自咬症疾病行为观察及防治技术试验.家畜生态,19(3):13-15
李继硕.2002.神经科技基础.高等教育出版社: 1
李静,刘班,刘成玉. 2006.红细胞膜脂质过氧化损伤及其作用机制.青岛大学医学院院报, 42(1):90-92
李钦民,韩真.2006.茶多酚对雷公藤内酯醇致小鼠肝损害的保护作用.世界华人消化杂志,14(9): 908-911
李巍.2005.毛皮动物自咬症的防制.贵州畜牧兽医, 29(3):27
李玉梅,白秀娟.2007.水貂自咬症的研究进展.经济动物学报,11(3):165-167
李云庆.2003.神经科学基础实习指导.第四军医大学出版社:6
李倬.2001.情绪表露对大鼠脑组织脂质过氧化作用及5-HT的影响.动物科学与动物医学, 6:20-21
刘玉萍.1993.亚硒酸钠维生素E混合制剂治疗蓝狐自咬症.中国兽医杂志,19(7):29
刘振玉.1995.谷胱甘肽的研究与应用.生命的化学,15(1):19-21
刘志发,吴醒身,周正谋,等.1999.大鼠缺血时血与脑中一氧化氮、超氧化物歧化酶和丙二醛含量的变化.中华航海医学杂志,6(2):97
彭国光,董为伟.2003.帕金森病神经保护性治疗研究进展.中华老年医学杂志,22(8):505-507
邵莹,张丽,郑连东.2006.过氧化脂质超氧化物歧化酶与中药治疗冠心病研究进展.现代中西医结合杂志, 15(7):970-971
施静,张静,刘晓春.1999.电针对局灶性脑缺血再灌注大鼠大脑皮层一氧化氮的影响.针刺研究,24(4):268
宋怀恩,闻韧.2003.抗氧化剂筛选方法的研究进展.中国药物化学杂志,13(2):119
孙得发,贾康胜,王建华.2006.毛皮动物自咬症与大脑神经细胞脂质过氧化关系初步分析.经济动物学报,4:242-247
孙得发,王建华,徐秀容,张志民,曹达江.2010.自咬症水貂神经系统病理组织学研究.西北农林科技大学学报,38(9):25-31
王爱国,冉鹏,周明辉.2002.氟中毒氧化应激与细胞凋亡关系的研究.中国公共卫生,18(6):68l-682
王胜军,迟兆富. 2007.癫痫持续状态与神经细胞程序性死亡.临床神经病学杂志,20(4):318-319
王维恩.1999.蓝狐自咬症的诊治.青海畜牧兽医杂志,29(4):32
许思思,宋金明,袁华茂等. 2010.镉、汞、铅和石油烃复合污染对渤海湾常见渔业资源生物的影响初探.生态毒理学报, 5(6):793-802
余雷晴.1984.水貂自咬症与微量元素.毛皮动物饲养. 2:1-3
余孝颖,吕锋洲,郑宝山.1999.砷中毒病区腐植酸对脂质过氧化反应的影响.中华预防医学杂志, 1:26-29
张弋,许松青,江慧琳,陈敏生.2003.纳洛酮对犬缺血再灌注损伤肺组织的MDA、SOD、NO的影响.广州医学院学报,31(3):48-50
郑云郎.1995.谷胱甘肽的生物学功能.生物学通报,30(5):22-24
Ahamed M M, Siddiqui K.2007. Low level lead exposure and oxidative stress: current opinions. Clin Chim Acta, 338:57–64
Al-Gadani Y, El-Ansary A, Attas O, Al-Ayadhi L. 2009.Metabolic biomarkers related to oxidative stress and antioxidant status in Saudi autistic children. Clinical Biochemistry, 42 (10-11): 1032–1040
Angkeow P,Deshpande S S,Qi B,et a1.2002. Redox factor-I:an extra-nuclear role in the regulation of endothelial oxidative stress and apoptosis.Cell Death & Differentiation, 9:7l7-725
Anuradha C D,Kanno S,Hirano S.2001. Oxidative damage to mitochondria is a preliminary step to caspase-3 activation in fluoride-induced apoptosis in HL-60 cells.Free Radic Biol Med, 31(3):367-73
Aymeric Rivollier, Laure Perrin-Cocon, Sylvie Luche, et al. 2006.High expression of antioxidant proteins in dendritic cells. Molecular & Cellular Proteomics, 5(4): 726-736
Baghdadli A, Pascal C, Grisi S, Aussilloux C. 2003.Risk factors for self-injurious behaviours among 222 young children with autistic disorders. Journal of Intellectual Disability Research ,47(8): 622-627
Beck M A .1999.Selenium and host defence towards viruses. Proc Nutr Soc, 58(3):7O7-7ll
Beyersmann D A, Hartwig.2008. Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms. Arch Toxicol, 82:493–512
Bian S B, Elliott R, Immig I, Sun D F. 2007.The influence ofβ-carotene supplementation on post-partum disease and subsequent reproductive performance of dairy cows in China. Journal of Animal and Feed Sciences, 16, Suppl. 2: 370–375
Bildsoe M, Heller K E,Jeppesen L L. 1990a. Stereotypies in adult ranch mink. Scientifur, 14:169-177 Bildsoe M, Heller K E, L L. 1990b.Stereotypies in female ranch mink: seasonal and diurnal variations. Scientifur,14: 243–247
Block M L, Wu X, Pei Z, Li G, Wang T, Qin L, Wilson B, Yan J, Hong J S. Boll M C, Alcaraz-Zubeldia M, Montes S, Rios C. 2008.Free copper, ferroxidase and SOD1 activities, lipid peroxidation and NO(x) content in the CSF. A different marker profile in four neurodegenerative diseases. Neurochemical Research, 33(9): 1717-1723
Borsting C F, Engherg R M. 1994.Inclusion of oxidized fish oil in mink diets. I.The influence on nutrient digestibility and fatty acid accumulation in tissues. J Anim Phys Anim Nutr, 72(2-3):132-145
Bottje, W G, Enkvetchakul, B. Moore, R. 1995.Effect of -tocopherol on antioxidants, Lipid peroxidation, and the incidence of pulmonary hypertension syndrome (Ascites) in broilers. Poultry Science ,74:1356-1369
Brigelius-Flohe R,Kelly F J,Salonen J T,et a1.2002.The European perspective on vitamin E:current knowledge and future research.American Journal of Clinical Nutrition,76(4): 703-716
Bryan H. King, Howard C. Cromwell, Hoa T. et al. 1998.Dopaminergic and Glutamatergic Interactions in the Expression of Self-Injurious. Behavior Developmental Neuroscience, 20:180-187Buege J A and Aust S D. 1978.Microsomal lipid peroxidation. Methods Enzymol, 52: 302–310
Calderón-Garciduenas, Solt L, Henríquez-Roldán A C.et al. 2008.Long-term air pollution exposure is associated with neuroinflammation,an altered innate immune response, disruption of the blood–brain barrier,ultrafine particulate deposition, and accumulation of amyloid beta-42 and alpha-synuclein in children and young adults. Toxicol Pathol,36: 289–310
Carmody R J,Cotter T G. 2000.Oxidative stress induces caspase—independent retinal apoptosis in vitro.Cell Death Diferentiation,7:282-29l
Casado A, Encarnación López-Fernández M, Concepción Casado M. 2008. Lipid peroxidation and antioxidant enzyme activities in vascular and Alzheimer dementias. Neurochemical Research,33(3): 450-458
Castilho R F, Carvalho-Alves P C, Vercesi A E, Ferreira S T. 1996.Oxidative damage to sarcoplasmic reticulum Ca2+-pump induced by Fe2+/H2O2/ascorbate is not mediated by lipid peroxidation or thiol oxidation and leads to protein fragmentation. Molecular and Cellular Biochemistry,159(2): 105–114
Cauwels R G, Martens L C.2005. Self-mutilation behaviour in Lesch-Nyhan syndrome. Journal of Oral Pathology & Medicine,34(9): 573-575
Caylak E, Aytekin M, Halifeoglu I. 2008. Antioxidant effects ofmethionine, lipoic acid, N-acetylcysteine and homocysteine on lead-induced oxidative stress to erythrocytes in rats. Exp Toxicol Pathol,60: 289–294 Chabrier P E, Demerle-Pallardy C, Auguet M. 1999.Nitric oxide synthases: targets for therapeutic strategies in neurological diseases. Cell Mol Life Sci,55:1029–1035
Chauhan A, Chauhan V.2006. Oxidative stress in autism. Pathophysiology,13(3): 71-81
Chen C, Arjomandi M, Balmes J. et al.2007.Effects of chronic and acute ozone exposure on lipid peroxidation and antioxidant capacity in healthy young adults. Environ Health Perspect, 115 :1732–1737
Cho V, Bannai S. 1990.Uptake of glutamate and cysteine in c-6 glioma cells and in cultured astrocytes. Journal of Neurochemistry,55(6):2091–2097
Choudhary S,Zhang W,Zhou F,et a1.2002.Cellular lipid peroxidation endroducts induce apoptosis in human lens epithelial cells. Free Radic Bio Med, 32:36O-369
Christine C,Winterbourna, Martin J D. Bonhamb, Hendrikje Bussa, Fikri M, Abu-Zidanb, John A, Windsorb. 2003. Elevated Protein Carbonyls as Plasma Markers of Oxidative Stress in Acute Pancreatitis. Pancreatology,3: 375-382
Clemens A, Schmitt, Scott W, Lowe.1999.Apoptosis and therapy.J Patho,187:l27-l37
CoppedèF M, Mancuso G, Siciliano L, Migliore L, Murri.2006. Genes and the environment in neurodegeneration. Biosci. Rep,26: 341–367
Crichton R R, Dexter D T, Ward R J. 2008. Metal based neurodegenerative diseases—from molecular mechanisms to therapeutic strategies. Coord Chem Rev, 252 : 1189–1199
David S. Cassarino, Christopher P, Fall, Russell H. et al. 1997.Elevated reactive oxygen species and antioxidant enzyme activities in animal and cellular models of Parkinson's disease. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease,1362(1): 77-86
Díaz-Cruz A, Nava C, Villanueva R, Serret M, Guinzberg R. 2008. Hepatic and cardiac oxidative stress and other metabolic changes in broilers with the ascites syndrome diseases. Brain Nerve, 60:157–170
Drechsel D A, Patel M. 2008.Role of reactive oxygen species in the neurotoxicity of environmental agents implicated in Parkinson’s disease. Free Radic Biol Med, 44: 1873–1886
Edwards T, Myers J.2007. Environmental exposures and gene regulation in disease etiology, Environ. Health Perspect, 115:1264–1270
Engherg R M, Borsting C F. 1994.Inclusion of oxidized fish oil in mink diets. 2. The influence on performance and health considering histopathological, clinical-chemical, and haematological indices. J Anim physiol Anim Nutr, 72:146-157
Fahn S, Cohen G. 1992.The oxidant stress hypothesis in Parkinson's disease: evidence supporting it. Annals of neurology,32(6): 804-812
Falk J L. 1971.The nature and determinants of adjunctive behavior. Physiol. Behav, (6): 577–588 Garrel C, Ceballos-Picot I, Germain G, Al-Gubory K H. 2007. Oxidative stress-inucible antioxidant adaptive response during prostaglandin F-2 alpha-induced luteal cell death in vivo. Free radical research, 41(3), 251-259
Geier D A, Ken J K, Graver C R, Adams J B. 2009.Biomarkers of environmental toxicity and susceptibility in autism. Journal of Neurological Sciences, 280(1-2): 127-128
G?tz M E, Freyberger A, Riederer P. 1990. Oxidative stress: a role in the pathogenesis of Parkinson's disease. Journal of Neural Transmission, 29 (Suppl): 241-249
Grover A K, Samson S E, Fomin V P. 1992.Peroxide inactivates calcium pumps in pig coronary artery. American Journal of Physiology, 263(2), 537–543
Grover A K, Samson S E. 1988.Effect of superoxide radical on Ca2+ pumps of coronary artery. American Journal of Physiology 255(3), 297–303
Gu F, Zhu M, Shi J, Hu Y, Zhao Z. 2008.Enhanced oxidative stress is an early event during development of Alzheimer-like pathologies in presenilin conditional knock-out mice. Neuroscience Letters ,440(1): 44-48 Guo J L, Zheng Q H, Yin Q Q. et al. 2007.Study on Mechanism of Ascites Syndrome of Broilers. American Journal of Animal and Veterinary Sciences,2(3): 62-65
Hall A V, Antoniou H,Wang Y, et a1.1994.Structural organization of the Hansen C P B. 1993.Stereotypies in ranch mink: The effect of genes, litter size and neighbours. Behavioural Processes,29:165～177
Hansen S W, Malmkvist J, Palme R, et al. 2007.Do double cages and access to occupational materials improve the welfare of farmed mink. Anim Welfare, 16(1): 63–76
Han-Yao Huang, Lawrence J, Appel, Kevin D, Croft, Edgar R, Miller. 2002.Effects of vitamin C and vitamin E on in vivo lipid peroxidation: results of a randomized controlled trial. American Journal of Clinical Nutrition,76(3): 549～555
Hirota K and Lambert D G. 1997. A comparative study of L-type voltage sensitive Ca2+ channels in rat brain regions and cultured neuronal cells. Neurosci Lett, 223:169-172
Hyman P, Oliver C, Hall S.2002. Self-injurious behavior, self-restraint, and compulsive behaviors in Cornelia de Lange syndrome. American Journal Of Mental Retardation ,107(2): 146-154
Iqbal, M Pumford, N R Tang, Z X Lassiter K ,Wing T, et al. 2004.Low feed efficient broilers within a single genetic line exhibit higher oxidative stress and protein expression in breast muscle with lower mitochondrial complex activity. Poultry Science, 83(3):474-484
Ishisaka R,Utsumi K,Utsumi T.2002.Involvement of lysosomal cysteine protease in hydrogen pe roxide induced apoptosis in HL-60 ceHs.Biosci Bio-technol Biochem,66(9):l865-l872
Jambrina E,Alonso R,Alcalde M,et,a1.2003. Calcium influxthrough receptor—operated channel inducesmitochondria -triggered paraptotic cell death.Biol Chem,278:14134-14145
Jeppesen L L, Heller K E, Dalsgaard T.2000. Effects of early weaning and housing conditions on the development of stereotypies in farmed mink. Applied Animal Behavioural Science, 68: 85-92
Jha N, Jurma O, Lalli G, Liu Y, Pettus E H, et al. 2000. Glutathione depletion in PC12 results in selective inhibition of mitochondrial complex I activity:Implications for Parkinson's disease. The Journal of Biological Chemistry,275(34): 26096-26101
Jinnah H A, Yitta S, Drew T, Kim B S, et al.1999. Calcium channel activation and self-biting in mice Neurobiology, 96(26):15228-15232
Jirasak, Wong-ekkabut J, Xu Z, et al.2007. Effect of lipid peroxidation on the properties of lipid bilayers: a molecular dynamics study. Biophys J, 93(12):4225-36
Jonge, G. 1989. Genetics and evolution of tail-biting by mink. Fur Rancher, 69: 5-6
Jorgensen M J, Kinsey J H, Novak M A.1998. Risk factors for self-injurious behavior in captive rhesus monkeys (Macaca mulatta). American Journal of Primatology,45: 187 (Abstract)
Keller J N, Schmitt F,Scheff S W, et al.1993. More rapid biochemical diagnosis of myocardial infarction: necessary? Prudent? Cost effective? Clin Chem, 39:1567-1569
King B H, Au D, Poland R E. 1995. Pretreatment with MK-801 inhibits pemoline-induced self-biting behavior in prepubertal rats. Dev Neurosci, 17(1):47-52
King B H, Au D, Poland R E. 1982. Self-biting behavior in prepubertal rats. Pharmacol Biochem Behav,17(4):613-617
Kita T, Miyazaki I, Asanuma M, Takeshima M, Wagner G C.2009. Dopamine-induced behavioral changes and oxidative stress in methamphetamine-induced neurotoxicity. International Review of Neurobiology 88: 43-64.
Kraemer G W, Clarke A S. 1990.The behavioral neurobiology of self-injurious behavior in rhesus monkeys.Progress in Neuro-Psychopharmacology & Biological Psychiatry,14 (Suppl):141-168
Kraemer G W, Schmidt D E, Ebert M H. 1997.The behavioral neurobiology of self-injurious behavior in rhesus monkeys. Current concepts and relations to impulsive behavior in humans. Annals of the New York Academy of Sciences, 836(1):12-38
Kuloglu M, Atmaca M, Tezcan E, Ustundag B, Bulut S.2002.Antioxidant enzyme and malondialdehyde levels in patients with panic disorder. Neuropsychobiology, 46(4):186-189
Kuloglu M, Ustundag B, Atmaca M, Canatan H, Tezcan A E, Cinkilinc N. 2002. Lipid peroxidation and antioxidant enzyme levels in patients with schizophrenia and bipolar disorder. Cell Biochemistry and Function,20(2):171-175
Kunz M, Gama C S, Andreazza A C, Salvador M, Ceresér K M, Gomes F A, Belmonte-de-Abreu P S, Berk M, Kapczinski F. 2008. Elevated serum superoxide dismutase and thiobarbituric acid reactive substances in different phases of bipolar disorder and in schizophrenia. Progress in Neuro-Psychopharmacology & Biological Psychiatry ,32(7):1677-1681
Lawrence A B, Terlow E M C. 1993.A review of behavioral factors involved in the development and continued performance of stereotypic behaviors in pigs. Journal of Animal Science, 71: 2815–2825 Lennon S V,Martin S J,Cotter T G.1991. Dose-dependent induction of apaptosis in human tumor or cell lines by widely diverging stiumuli.Cell Prolif,l24:2O3-2l4
Levine R L, Garland D, Oliver C N, Amici A, Climent I, Lenzi A. 1990.Determination of carbonyl contentin oxidatively modified proteins. Methods Enzymol,186: 464–478
Line S W, Morgan K N, Markowitz H, Riddell M. 1990. Behavioral responses of female longtailed macaques (Macaca fascicularis) to pair formation. Laboratory Primate Newsletter, 29(4): 1-5
Lotharius J,Dugan L L, O’Malley K L.1999.Distinct Mechanisms Underlie Neurotoxin-Mediated Cell Death in Cultured Dopaminergic Neurons. J Neuro Sci, 19(4):l284-1293
Lovell M A, Markesbery W R. 2007.Oxidative DNA damage in mild cognitive impairment and late-stage Alzheimer’s disease. Nucleic Acids Res,35:7497–7504.
Lovell M A, Robertson J D, Teesdale W M.et al. 1998.Copper, iron and zinc in Alzheimer’s disease senile plaques. J Neurol Sci, 158: 47–52
Machlin L J. Bendich A.1987. Free radical tissue damage: protective role of antioxidant nutrients.FASEB J, 1:441-445
Malis C D,Bonventre J V.1986.Mechanism of calcium potentiation of oxygen free radical injury to renalmitochondria.A model for-post-ischemic and toxic mitochondrial damage.Biol Chem,261:14201-14208
Malmkvist J and Hansen S W. 2001.The welfare of farmed mink (Mustela vison) in relation to behavioural selection: A review. Animal Welfare,10: 41-52
Mancuso M. CoppedèF. Migliore L. Siciliano G. Murri L.2006.Mitochondrial dysfunction,oxidative stress and neurodegeneration, J Alzheimers Dis. 14:59-73
Marcus D L, Thomas C, Rodriguez C, Simberkoff K, Tsai J S, et al.1998. Increased peroxidation and reduced antioxidant enzyme activity in Alzheimer's disease. Experimental Neurology,150(1):40-44
Mason G J, Cooper C, Clarebrough C. 2001. The welfare of fur-farmed mink. Nature, 410:35-36
Mason G J. 1993.Age and context affect the stereotypies of caged mink. Behaviour, 127:191-229
Mason G J. 1995.Tail-biting in mink (Mustela vison) is influenced by age at removal from the mother. Animal Welfare, 3:305-311.
Mason GJ. 1991.Stereotypy: a critical review. Animal Behavior, 41: 1015–1038. Mason k E, Hartsouggh R. 1951.“Steatitis”or“yellow fat”in mink, and its relation to dietary fats and inadequacy of vitamin E. J Am Vet Med Assoc 119:72-75
Mason, G J. 1994.Tail-biting in mink (Mustela vison) is in?uenced by age at removal from the mother. Animal Welfare, 3(4), 305–311
Mason, G. J. 1992.Stereotypy and welfare in mink. J. Anim. Sci. 70:(suppl.1):158.
Mason, G. J. 1993.Age and context affect the stereotypies of caged mink. Behaviour, 127:191-229
Mason,G J. 1996.Early weaning enhances later development of stereotypy in mink. In: Duncan IJH, Widowski T, Haley DB (Eds). Proceedings of the 30th International Congress of the International Society for Applied Ethology:16
Mathews C A, Waller J, Glidden D, Lowe T L, Herrera L D, Budman C L, Erenberg G, Naarden A, Bruun R D, Freimer N B, Reus V I. 2004. Self injurious behaviour in Tourette syndrome: correlates with impulsivity and impulse control. Journal of Neurology, Neurosurgery and Psychiatry,75(8): 149-1155
Migliore L, Fontana I, Trippi F, Colognato R, CoppedèF, Tognoni G, Nucciarone B, Siciliano G. 2005. Oxidative DNA damage in peripheral leukocytes of mild cognitive impairment and AD patients. Neurobiol Aging, 26(5):567-73
Migliore, L. Fontana, I. Colognato, R. et al. 2005. Searching for the role and themost suitable biomarkersof oxidative stress in Alzheimer’s disease and in other neurodegenerative diseases. Neurobiol, 26:587–595 Mirella T,Marco G,Angelo C,et a1.2002.A P53一P66shc signaling pathway controls intracellular redox status.1evels of oxidation damaged DNA and oxidative stress induced apoptosis. Oncogene,21: 3872-3878
Morgan K, Tromborg C. 2007.Sources of stress in captivity. Applied Animal Behaviour Science, 102(3): 262-302
Mori, Tomohisa; Ito, Shinobu; Kita, Taizo; Narita, Minoru; Suzuki, Tsutomu; Matsubayashi, Kenji; Sawaguchi, Toshiko. 2007.Oxidative stress in methamphetamine-induced self-injurious behavior in mice. Behavioural Pharmacology, 18(3 ):239-249
Mueller K, Nyhan W L. 1980. Pharmacologic control of pemoline induced self-injurious behavior in rats. Pharmacol Biochem Behav,13(5):627-31
Mueller K, Hollingsworth E, Pettit H. 1986.Repeated pemoline produces self-injurious behavior in adult and weanling rats. Pharmacol Biochem Behav,25(5):933-938
Mueller K, Nyhan WL. 1982. Pharmacologic control of pemoline induced self-injurious behavior in rats. Pharmacol Biochem Behav,16(6):957-963
Mueller K, Saboda S, Palmour R, et al. 1998.Self-injurious behavior produced in rats by daily caffeine and continuous amphetamine.Dev Neurosci, 20(2/3):180-187
Nemmiche S, Chabane-Sari D, Guiraud P.2007. Role of alpha-tocopherol in cadmium-induced oxidative stress in Wistar rat's blood, liver and brain. Chemico-Biological Interactions ,170(3): 221-230
Ning Ke,Wang Zheng-Guo,Chen Chang Cai,Li Jinming,Zhu Peifang. 1999.Effects of excitatory amino acids and nimodipine on calcium currents in cultured rat cortical neurons.中国药理学报,20(4):329-333
Novgorodov S A,Gogvadze V G,Medvedeve B J,et,a1.1989. The effect of butylated hydr-oxytoluene,an inhibitor of lipid peroxidation on the calcium-induced uncoupling of rat liver mitochondria.FEBS Lett,248(1-2):179—181
Ookawara T, Matsuura N, Oh-ishi T, Okazaki M, Kizaki T, Suzuki K, Hitomi Y, Suzuki K, Ohno H. 2000. Serum extracellular superoxide dismutase in pediatric patients with various diseases as judged by an ELISA. Research Communications in Molecular Pathology & Pharmacology 107(3-4):291-296
Ozaki M ,Deshpande S S,Angkeow P,et a1 . 2000. Inhibition of the Racl GT-Pase protects against nonlethal ischrmitdreped'usion-induced necrosis and apoptosis in vivo.FASEB J,14:4l8-429
Pacifici R E, Davies K J. 1991.Protein, lipid and DNA repair systems in oxidative stress: the free-radical theory of aging revisited. Gerontology , 37(1-3):166-80.
Qureshi G A, Qureshi A A, Memon S A, Parvez S H.2006. Impact of selenium, iron,copper and zinc in on/off Parkinson’s patients on l-dopa therapy. J Neural Transm, Suppl. 71 :229–236
Qureshi, G A (Eds.). 2007.Oxidative Stress and Neurodegenerative Disorders. Elsevier Science Reinhardt V. 1994. Pair-housing rather than single-housing for laboratory rhesus macaques. Journal of Medical Primatology,23: 426-431
Rushen J P. 1985.Stereotypies aggression and the feeding schedules of tethered sows. Appl Anim Behav Sci,14: 137–147
Sahakian B J, Robbins T W, Morgan M J, Iversen S D.1975.The effects of psychomotor stimulants on stereotypy and locomotor activity in socially-deprived and control rats. Brain Research, 84: 195–205
Sallman H P, Drommer W, Solaro K L.1988. Pathogenic and metabolic impact on broilers strained by oxidized fats. Israel Journal of Veterinary Medicine,44(3):183-194
Sansom D, Krishnan V H, Corbett J, Kerr A.1993. Emotional and behavioural aspects of Rett syndrome,35(4): 340-345
Sara P D and Richard W J. 2004.Genetic and environmental factors modulating serum concentrations and activities of the antioxidant enzyme paraoxonase-1. Clinical Science , 107:435–447
Scherer N M, Deamer D W.1986. Oxidative stress impairs the function of sarcoplasmic reticulum by oxidation of sulfhydryl groups in the Ca2+-ATPase. Archives of Biochemistry and Biophysics,246(2):589–601
Schuessel K, Sch?fer S, Bayer T A, Czech C, Pradier L, Müller-Spahn F, Müller W E, Eckert A.2005. Impaired Cu/Zn-SOD activity contributes to increased oxidative damage in APP transgenic mice. Neurobiology of Disease,18(1):89-99
Suhail Kasim, H.A. Jinnah .2003.Self-Biting Induced by Activation of L-Type Calcium Channels in Mice: Dopaminergic Influences.Dev Neurosci, 25:20-25
Sheldon B W ,Curtis P A,Dawson P L,et a1.1997.Effect of dietary vitam in E on the oxidative stability,flavour,colour and volatile profiles of refrigerated and frozen turkey breast meat.Poultry Science,76:634—641
Shen H M, Shi C Y, Lee H P, Ong C N.1994. Aflatoxin B1-induced lipid peroxidation in rat liver. Toxicol. Appl. Pharmacol, 127: 145-150
Shibata, N. Kobayashi, M. 2008.The role for oxidative stress in neurodegenerative diseases. Brain Nerve, 60(2):157-70
Simeon D, Stanley B, Frances A et al.1992. Self-mutilation in personality disorders: psychological and biological correlates. Am J Psychiatry,149(2):221-226
Singh R,Kaur B,Kalina I, Popov T A, et al.2007. Effects of environmental air pollution on endogenous oxidative DNA damage in humans, Mutat Res,620:71–82
Skovgaard K, Jeppesen L L, Hansen C P B.1997. The effect of swimming water and cage size on the behaviour of ranch mink (Mustela vison). Scientifur ,(21): 253 - 260
Skulachev V P.1999. Mitochondrial physiology and pathology; concepts of programmed death of organelles, cells and organisms, Mol Aspects Med, 20:139–184
Slater T F, Cheeseman K H,Davies M J, et al.1987. Free radical mechanisms in relation to tissue injury. Proceedings of the Nutrition Society ,46:1-12
S?derstr?m S, Fredriksson A, Dencker L, et al.1995.The effect of mercury vapour on cholinergic neurons in the fetal brain: studies on the expression of nerve growth factor and its low-and high-affinity receptors.Brain research.Developmental brain research,85(1):96-108
Sofic E, Lange K W, Jellinger K, Riederer P.1992. Reduced and oxidized glutathione in the substantia nigra of patients with Parkinson's disease. Neuroscience Letters,142 (2): 128-30
Staci D, Kies and Darragh P. 1982. Self-injurious behaviour: a comparison of caffeine and pemoline models in rats. Pharmacol Biochem Behav, 16(6):957-63
Stringari J A K C,Nunes J L, Franco D, Bohrer S C, Garcia A L C,Dafre Milatovic D O, Souza J B T, Rocha M, Aschner M, Farina.2008.Prenatal methylmercury exposure hampes glutathione antioxidant system ontogenesis and causes long-lasting oxidative stress in the mouse brain. Toxicol ApplPharmacol,227 :147–154
Suhail Kasim H A, Jinnah.2003. Self-Biting induced by activation of L-Type calcium channels in mice: dopaminergic influences. Developmental Neuroscience, (25):20-25
Sun Y, Oberley L W and Li Y. 1988.A simple method for clinical assay of superoxide dismutase. Clinical Chemistry, 34(3):497–500
Thome J, Gsell W, R?sler M, Kornhuber J, Fr?lich L, Hashimoto E,et al.1997.Oxidative-stress associated parameters (lactoferrin, superoxide dismutases) in serum of patients with Alzheimer's disease. Life Sciences ,60(1):13-19
Tinsley N, Iqbal M, Pumford N R, et al.2010. Investigation of mitochondrial protein expression and oxidation in heart muscle in low and high feed efficient male broilers in a single genetic line1. Poult Sci,89:349-352
Traber M G, Atkinson J. 2007.Vitamin E .Antioxidant and nothing more. Free Radical Biology and Medicine,43(1): 4–15
Verhasselt V, Goldman M, Willems F.1998. Oxidative stress up-regulates IL-8 and TNF-alpha synthesis by human dendritic cells. European Journal of Immunology, 28(11): 3886-3890
Veronesi B.2004. Nanometer size diesel exhaust particles are selectively toxic to dopaminergic neurons: the role of microglia, phagocytosis, and NADPH oxidase, FASEB, 18 :1618–1620
Villalba R, Harrington C J.2000. Repetitive self-injurious behavior: a neuropsychiatric perspective and review of pharmacologic treatments. Semin Clin Neuropsychiatry ,5(4):215-226
Vinke C M, Eenkhoorn N C, Netto W J, Fermont P C J, Spruijt B M. 2002.Stereotypic behaviour and tail biting in farmed mink (Mustela Vison) in a new housing system. Animal Welfare,11(2): 231-245
Vinke C M, Vanden Bos R, Spruijt B M.2004. Anticipatory activity and stereotypical behaviour in American mink (Mustela vison) in three housing systems differing in the amount of enrichments. Applied Animal Behaviour Science,89 (1-2): 145-161
Visser J E, Smith D W, Moy S S, Breese G R, Friedmann T, Rothstein J D, Jinnah HA.2002.Oxidative stress and dopamine deficiency in a genetic mouse model of Lesch-Nyhan disease. Developmental Brain Research,133(2):127-39
Vojdani A, Bock K, Hirani A K.2008. Low natural killer cell cytotoxic activity in autism: the role of glutathion, IL-2 and IL-15. Journal of Neuroimmunology, 205(1–2):148–154
Wander R C, Du S, Ketchum S O, Rowe K E. 1996.α-Tocopherol influences in vivo indices of lipid peroxidation in postmenopausal women given fish oil. J Nutr, 126:643–652
Wang Z, Bunce G E, Hess J L. 1993.Selenite and Ca2+ homeostasis in the rat lens: effect on Ca-ATPase and passive Ca2+ transport. Current Eye Research ,12(3):213–218
Waschulewski I H , Sunde R A.1988. Effect of dietary methionine on tissue selenium and glutathione peroxidase (EC 1.11.1.9) activity in rats given selenomethionine. Br J Nutr, 60(1):57-68
Waschulewski I H,Sunde R A.1998. Effect of dietary methionine on utilization of tissue selenium from dietary selenomethionine for glutathione peroxidase in the rat. J Nutr, 1118(3):367-374
Wong-Ekkabut J, Xu Z, Triampo W, Tang I M, Tieleman D P, Monticelli L.2007. Effect of lipid peroxidation on the properties of lipid bilayers: a molecular dynamics study. Biophysical journal ,93(12):4225-4236
Wu G,Fang Y Z,Yang S,et a1.2004.Glutathione metabolism and its implications for hea1th.J Nutr,134(3):489-492
Xie J, Fan R, Meng Z.2007. Protein oxidation and DNA–protein crosslink induced by sulfur dioxide in lungs, livers, and hearts from mice, Inhal Toxicol,19: 759–765
Young J F,Stagsted J ,Jensen S K, Karlsson A H, et al.2003. Ascorbic acid, alpha-tocopherol, and oregano supplements reduce stress-induced deterioration of chicken meat quality. Poultry Science,82( 8): 1343-1351
Zaidi S M, Naheed Banu. 2004. Antioxidant potential of vitamins A, E and C in modulating oxidative stress in rat brain. Clinica Chimica Acta,340(1-2): 229–233
Zhang X Y, Zhou D F, Qi L Y, Chen S, Cao L Y, Chen D C, Xiu M H, Wang F, Wu G Y, Lu L, Kosten T A, Kosten T R.2009.Superoxide dismutase and cytokines in chronic patients with schizophrenia: association with psychopathology and response to antipsychotics. Psychopharmacology, 204(1): 177-184
董为伟.2002.神经保护的基础与临床.北京:科学出版社:14-21
高宏伟,陈维岩,马振凯.1995.水貂自咬症研究概况.毛皮动物饲养,3:41-43
高宏伟,陈维岩.1994.自咬症水貂脑、肝、肾和毛中汞残留量的分析.毛皮动物饲养, 2:1-3
高颖,许彩民,杨洋.1998.氧化诱导K652细胞凋亡机制的初步探讨.中国生物化学与分子生物学学报,14(3):295-299
胡蓉玲,张淑珍.2004.蓝狐自咬症的诊治.中国动物保健,10:29-30
江勇. 1998.汞对内耳及神经系统的毒性作用.黑龙江畜牧兽医, 2:161-163
井明艳,赵树盛,付亮剑. 2006.硒的生化特性与谷胱甘肽系统.饲料工业,4:8-11
李长胜.1998.狐貉自咬症疾病行为观察及防治技术试验.家畜生态,19(3):13-15
李继硕.2002.神经科技基础.高等教育出版社: 1
李静,刘班,刘成玉. 2006.红细胞膜脂质过氧化损伤及其作用机制.青岛大学医学院院报, 42(1):90-92
李钦民,韩真.2006.茶多酚对雷公藤内酯醇致小鼠肝损害的保护作用.世界华人消化杂志,14(9): 908-911
李巍.2005.毛皮动物自咬症的防制.贵州畜牧兽医, 29(3):27
李玉梅,白秀娟.2007.水貂自咬症的研究进展.经济动物学报,11(3):165-167
李云庆.2003.神经科学基础实习指导.第四军医大学出版社:6
李倬.2001.情绪表露对大鼠脑组织脂质过氧化作用及5-HT的影响.动物科学与动物医学, 6:20-21
刘玉萍.1993.亚硒酸钠维生素E混合制剂治疗蓝狐自咬症.中国兽医杂志,19(7):29
刘振玉.1995.谷胱甘肽的研究与应用.生命的化学,15(1):19-21
刘志发,吴醒身,周正谋,等.1999.大鼠缺血时血与脑中一氧化氮、超氧化物歧化酶和丙二醛含量的变化.中华航海医学杂志,6(2):97
彭国光,董为伟.2003.帕金森病神经保护性治疗研究进展.中华老年医学杂志,22(8):505-507
邵莹,张丽,郑连东.2006.过氧化脂质超氧化物歧化酶与中药治疗冠心病研究进展.现代中西医结合杂志, 15(7):970-971
施静,张静,刘晓春.1999.电针对局灶性脑缺血再灌注大鼠大脑皮层一氧化氮的影响.针刺研究,24(4):268
宋怀恩,闻韧.2003.抗氧化剂筛选方法的研究进展.中国药物化学杂志,13(2):119
孙得发,贾康胜,王建华.2006.毛皮动物自咬症与大脑神经细胞脂质过氧化关系初步分析.经济动物学报,4:242-247
孙得发,王建华,徐秀容,张志民,曹达江.2010.自咬症水貂神经系统病理组织学研究.西北农林科技大学学报,38(9):25-31
王爱国,冉鹏,周明辉.2002.氟中毒氧化应激与细胞凋亡关系的研究.中国公共卫生,18(6):68l-682
王胜军,迟兆富. 2007.癫痫持续状态与神经细胞程序性死亡.临床神经病学杂志,20(4):318-319
王维恩.1999.蓝狐自咬症的诊治.青海畜牧兽医杂志,29(4):32
许思思,宋金明,袁华茂等. 2010.镉、汞、铅和石油烃复合污染对渤海湾常见渔业资源生物的影响初探.生态毒理学报, 5(6):793-802
余雷晴.1984.水貂自咬症与微量元素.毛皮动物饲养. 2:1-3
余孝颖,吕锋洲,郑宝山.1999.砷中毒病区腐植酸对脂质过氧化反应的影响.中华预防医学杂志, 1:26-29
张弋,许松青,江慧琳,陈敏生.2003.纳洛酮对犬缺血再灌注损伤肺组织的MDA、SOD、NO的影响.广州医学院学报,31(3):48-50
郑云郎.1995.谷胱甘肽的生物学功能.生物学通报,30(5):22-24
Ahamed M M, Siddiqui K.2007. Low level lead exposure and oxidative stress: current opinions. Clin Chim Acta, 338:57–64
Al-Gadani Y, El-Ansary A, Attas O, Al-Ayadhi L. 2009.Metabolic biomarkers related to oxidative stress and antioxidant status in Saudi autistic children. Clinical Biochemistry, 42 (10-11): 1032–1040
Angkeow P,Deshpande S S,Qi B,et a1.2002. Redox factor-I:an extra-nuclear role in the regulation of endothelial oxidative stress and apoptosis.Cell Death & Differentiation, 9:7l7-725
Anuradha C D,Kanno S,Hirano S.2001. Oxidative damage to mitochondria is a preliminary step to caspase-3 activation in fluoride-induced apoptosis in HL-60 cells.Free Radic Biol Med, 31(3):367-73
Aymeric Rivollier, Laure Perrin-Cocon, Sylvie Luche, et al. 2006.High expression of antioxidant proteins in dendritic cells. Molecular & Cellular Proteomics, 5(4): 726-736
Baghdadli A, Pascal C, Grisi S, Aussilloux C. 2003.Risk factors for self-injurious behaviours among 222 young children with autistic disorders. Journal of Intellectual Disability Research ,47(8): 622-627
Beck M A .1999.Selenium and host defence towards viruses. Proc Nutr Soc, 58(3):7O7-7ll
Beyersmann D A, Hartwig.2008. Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms. Arch Toxicol, 82:493–512
Bian S B, Elliott R, Immig I, Sun D F. 2007.The influence ofβ-carotene supplementation on post-partum disease and subsequent reproductive performance of dairy cows in China. Journal of Animal and Feed Sciences, 16, Suppl. 2: 370–375
Bildsoe M, Heller K E,Jeppesen L L. 1990a. Stereotypies in adult ranch mink. Scientifur, 14:169-177 Bildsoe M, Heller K E, L L. 1990b.Stereotypies in female ranch mink: seasonal and diurnal variations. Scientifur,14: 243–247
Block M L, Wu X, Pei Z, Li G, Wang T, Qin L, Wilson B, Yan J, Hong J S. Boll M C, Alcaraz-Zubeldia M, Montes S, Rios C. 2008.Free copper, ferroxidase and SOD1 activities, lipid peroxidation and NO(x) content in the CSF. A different marker profile in four neurodegenerative diseases. Neurochemical Research, 33(9): 1717-1723
Borsting C F, Engherg R M. 1994.Inclusion of oxidized fish oil in mink diets. I.The influence on nutrient digestibility and fatty acid accumulation in tissues. J Anim Phys Anim Nutr, 72(2-3):132-145
Bottje, W G, Enkvetchakul, B. Moore, R. 1995.Effect of -tocopherol on antioxidants, Lipid peroxidation, and the incidence of pulmonary hypertension syndrome (Ascites) in broilers. Poultry Science ,74:1356-1369
Brigelius-Flohe R,Kelly F J,Salonen J T,et a1.2002.The European perspective on vitamin E:current knowledge and future research.American Journal of Clinical Nutrition,76(4): 703-716
Bryan H. King, Howard C. Cromwell, Hoa T. et al. 1998.Dopaminergic and Glutamatergic Interactions in the Expression of Self-Injurious. Behavior Developmental Neuroscience, 20:180-187Buege J A and Aust S D. 1978.Microsomal lipid peroxidation. Methods Enzymol, 52: 302–310
Calderón-Garciduenas, Solt L, Henríquez-Roldán A C.et al. 2008.Long-term air pollution exposure is associated with neuroinflammation,an altered innate immune response, disruption of the blood–brain barrier,ultrafine particulate deposition, and accumulation of amyloid beta-42 and alpha-synuclein in children and young adults. Toxicol Pathol,36: 289–310
Carmody R J,Cotter T G. 2000.Oxidative stress induces caspase—independent retinal apoptosis in vitro.Cell Death Diferentiation,7:282-29l
Casado A, Encarnación López-Fernández M, Concepción Casado M. 2008. Lipid peroxidation and antioxidant enzyme activities in vascular and Alzheimer dementias. Neurochemical Research,33(3): 450-458
Castilho R F, Carvalho-Alves P C, Vercesi A E, Ferreira S T. 1996.Oxidative damage to sarcoplasmic reticulum Ca2+-pump induced by Fe2+/H2O2/ascorbate is not mediated by lipid peroxidation or thiol oxidation and leads to protein fragmentation. Molecular and Cellular Biochemistry,159(2): 105–114
Cauwels R G, Martens L C.2005. Self-mutilation behaviour in Lesch-Nyhan syndrome. Journal of Oral Pathology & Medicine,34(9): 573-575
Caylak E, Aytekin M, Halifeoglu I. 2008. Antioxidant effects ofmethionine, lipoic acid, N-acetylcysteine and homocysteine on lead-induced oxidative stress to erythrocytes in rats. Exp Toxicol Pathol,60: 289–294 Chabrier P E, Demerle-Pallardy C, Auguet M. 1999.Nitric oxide synthases: targets for therapeutic strategies in neurological diseases. Cell Mol Life Sci,55:1029–1035
Chauhan A, Chauhan V.2006. Oxidative stress in autism. Pathophysiology,13(3): 71-81
Chen C, Arjomandi M, Balmes J. et al.2007.Effects of chronic and acute ozone exposure on lipid peroxidation and antioxidant capacity in healthy young adults. Environ Health Perspect, 115 :1732–1737
Cho V, Bannai S. 1990.Uptake of glutamate and cysteine in c-6 glioma cells and in cultured astrocytes. Journal of Neurochemistry,55(6):2091–2097
Choudhary S,Zhang W,Zhou F,et a1.2002.Cellular lipid peroxidation endroducts induce apoptosis in human lens epithelial cells. Free Radic Bio Med, 32:36O-369
Christine C,Winterbourna, Martin J D. Bonhamb, Hendrikje Bussa, Fikri M, Abu-Zidanb, John A, Windsorb. 2003. Elevated Protein Carbonyls as Plasma Markers of Oxidative Stress in Acute Pancreatitis. Pancreatology,3: 375-382
Clemens A, Schmitt, Scott W, Lowe.1999.Apoptosis and therapy.J Patho,187:l27-l37
CoppedèF M, Mancuso G, Siciliano L, Migliore L, Murri.2006. Genes and the environment in neurodegeneration. Biosci. Rep,26: 341–367
Crichton R R, Dexter D T, Ward R J. 2008. Metal based neurodegenerative diseases—from molecular mechanisms to therapeutic strategies. Coord Chem Rev, 252 : 1189–1199
David S. Cassarino, Christopher P, Fall, Russell H. et al. 1997.Elevated reactive oxygen species and antioxidant enzyme activities in animal and cellular models of Parkinson's disease. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease,1362(1): 77-86
Díaz-Cruz A, Nava C, Villanueva R, Serret M, Guinzberg R. 2008. Hepatic and cardiac oxidative stress and other metabolic changes in broilers with the ascites syndrome diseases. Brain Nerve, 60:157–170
Drechsel D A, Patel M. 2008.Role of reactive oxygen species in the neurotoxicity of environmental agents implicated in Parkinson’s disease. Free Radic Biol Med, 44: 1873–1886
Edwards T, Myers J.2007. Environmental exposures and gene regulation in disease etiology, Environ. Health Perspect, 115:1264–1270
Engherg R M, Borsting C F. 1994.Inclusion of oxidized fish oil in mink diets. 2. The influence on performance and health considering histopathological, clinical-chemical, and haematological indices. J Anim physiol Anim Nutr, 72:146-157
Fahn S, Cohen G. 1992.The oxidant stress hypothesis in Parkinson's disease: evidence supporting it. Annals of neurology,32(6): 804-812
Falk J L. 1971.The nature and determinants of adjunctive behavior. Physiol. Behav, (6): 577–588 Garrel C, Ceballos-Picot I, Germain G, Al-Gubory K H. 2007. Oxidative stress-inucible antioxidant adaptive response during prostaglandin F-2 alpha-induced luteal cell death in vivo. Free radical research, 41(3), 251-259
Geier D A, Ken J K, Graver C R, Adams J B. 2009.Biomarkers of environmental toxicity and susceptibility in autism. Journal of Neurological Sciences, 280(1-2): 127-128
G?tz M E, Freyberger A, Riederer P. 1990. Oxidative stress: a role in the pathogenesis of Parkinson's disease. Journal of Neural Transmission, 29 (Suppl): 241-249
Grover A K, Samson S E, Fomin V P. 1992.Peroxide inactivates calcium pumps in pig coronary artery. American Journal of Physiology, 263(2), 537–543
Grover A K, Samson S E. 1988.Effect of superoxide radical on Ca2+ pumps of coronary artery. American Journal of Physiology 255(3), 297–303
Gu F, Zhu M, Shi J, Hu Y, Zhao Z. 2008.Enhanced oxidative stress is an early event during development of Alzheimer-like pathologies in presenilin conditional knock-out mice. Neuroscience Letters ,440(1): 44-48 Guo J L, Zheng Q H, Yin Q Q. et al. 2007.Study on Mechanism of Ascites Syndrome of Broilers. American Journal of Animal and Veterinary Sciences,2(3): 62-65
Hall A V, Antoniou H,Wang Y, et a1.1994.Structural organization of the Hansen C P B. 1993.Stereotypies in ranch mink: The effect of genes, litter size and neighbours. Behavioural Processes,29:165～177
Hansen S W, Malmkvist J, Palme R, et al. 2007.Do double cages and access to occupational materials improve the welfare of farmed mink. Anim Welfare, 16(1): 63–76
Han-Yao Huang, Lawrence J, Appel, Kevin D, Croft, Edgar R, Miller. 2002.Effects of vitamin C and vitamin E on in vivo lipid peroxidation: results of a randomized controlled trial. American Journal of Clinical Nutrition,76(3): 549～555
Hirota K and Lambert D G. 1997. A comparative study of L-type voltage sensitive Ca2+ channels in rat brain regions and cultured neuronal cells. Neurosci Lett, 223:169-172
Hyman P, Oliver C, Hall S.2002. Self-injurious behavior, self-restraint, and compulsive behaviors in Cornelia de Lange syndrome. American Journal Of Mental Retardation ,107(2): 146-154
Iqbal, M Pumford, N R Tang, Z X Lassiter K ,Wing T, et al. 2004.Low feed efficient broilers within a single genetic line exhibit higher oxidative stress and protein expression in breast muscle with lower mitochondrial complex activity. Poultry Science, 83(3):474-484
Ishisaka R,Utsumi K,Utsumi T.2002.Involvement of lysosomal cysteine protease in hydrogen pe roxide induced apoptosis in HL-60 ceHs.Biosci Bio-technol Biochem,66(9):l865-l872
Jambrina E,Alonso R,Alcalde M,et,a1.2003. Calcium influxthrough receptor—operated channel inducesmitochondria -triggered paraptotic cell death.Biol Chem,278:14134-14145
Jeppesen L L, Heller K E, Dalsgaard T.2000. Effects of early weaning and housing conditions on the development of stereotypies in farmed mink. Applied Animal Behavioural Science, 68: 85-92
Jha N, Jurma O, Lalli G, Liu Y, Pettus E H, et al. 2000. Glutathione depletion in PC12 results in selective inhibition of mitochondrial complex I activity:Implications for Parkinson's disease. The Journal of Biological Chemistry,275(34): 26096-26101
Jinnah H A, Yitta S, Drew T, Kim B S, et al.1999. Calcium channel activation and self-biting in mice Neurobiology, 96(26):15228-15232
Jirasak, Wong-ekkabut J, Xu Z, et al.2007. Effect of lipid peroxidation on the properties of lipid bilayers: a molecular dynamics study. Biophys J, 93(12):4225-36
Jonge, G. 1989. Genetics and evolution of tail-biting by mink. Fur Rancher, 69: 5-6
Jorgensen M J, Kinsey J H, Novak M A.1998. Risk factors for self-injurious behavior in captive rhesus monkeys (Macaca mulatta). American Journal of Primatology,45: 187 (Abstract)
Keller J N, Schmitt F,Scheff S W, et al.1993. More rapid biochemical diagnosis of myocardial infarction: necessary? Prudent? Cost effective? Clin Chem, 39:1567-1569
King B H, Au D, Poland R E. 1995. Pretreatment with MK-801 inhibits pemoline-induced self-biting behavior in prepubertal rats. Dev Neurosci, 17(1):47-52
King B H, Au D, Poland R E. 1982. Self-biting behavior in prepubertal rats. Pharmacol Biochem Behav,17(4):613-617
Kita T, Miyazaki I, Asanuma M, Takeshima M, Wagner G C.2009. Dopamine-induced behavioral changes and oxidative stress in methamphetamine-induced neurotoxicity. International Review of Neurobiology 88: 43-64.
Kraemer G W, Clarke A S. 1990.The behavioral neurobiology of self-injurious behavior in rhesus monkeys.Progress in Neuro-Psychopharmacology & Biological Psychiatry,14 (Suppl):141-168
Kraemer G W, Schmidt D E, Ebert M H. 1997.The behavioral neurobiology of self-injurious behavior in rhesus monkeys. Current concepts and relations to impulsive behavior in humans. Annals of the New York Academy of Sciences, 836(1):12-38
Kuloglu M, Atmaca M, Tezcan E, Ustundag B, Bulut S.2002.Antioxidant enzyme and malondialdehyde levels in patients with panic disorder. Neuropsychobiology, 46(4):186-189
Kuloglu M, Ustundag B, Atmaca M, Canatan H, Tezcan A E, Cinkilinc N. 2002. Lipid peroxidation and antioxidant enzyme levels in patients with schizophrenia and bipolar disorder. Cell Biochemistry and Function,20(2):171-175
Kunz M, Gama C S, Andreazza A C, Salvador M, Ceresér K M, Gomes F A, Belmonte-de-Abreu P S, Berk M, Kapczinski F. 2008. Elevated serum superoxide dismutase and thiobarbituric acid reactive substances in different phases of bipolar disorder and in schizophrenia. Progress in Neuro-Psychopharmacology & Biological Psychiatry ,32(7):1677-1681
Lawrence A B, Terlow E M C. 1993.A review of behavioral factors involved in the development and continued performance of stereotypic behaviors in pigs. Journal of Animal Science, 71: 2815–2825 Lennon S V,Martin S J,Cotter T G.1991. Dose-dependent induction of apaptosis in human tumor or cell lines by widely diverging stiumuli.Cell Prolif,l24:2O3-2l4
Levine R L, Garland D, Oliver C N, Amici A, Climent I, Lenzi A. 1990.Determination of carbonyl contentin oxidatively modified proteins. Methods Enzymol,186: 464–478
Line S W, Morgan K N, Markowitz H, Riddell M. 1990. Behavioral responses of female longtailed macaques (Macaca fascicularis) to pair formation. Laboratory Primate Newsletter, 29(4): 1-5
Lotharius J,Dugan L L, O’Malley K L.1999.Distinct Mechanisms Underlie Neurotoxin-Mediated Cell Death in Cultured Dopaminergic Neurons. J Neuro Sci, 19(4):l284-1293
Lovell M A, Markesbery W R. 2007.Oxidative DNA damage in mild cognitive impairment and late-stage Alzheimer’s disease. Nucleic Acids Res,35:7497–7504.
Lovell M A, Robertson J D, Teesdale W M.et al. 1998.Copper, iron and zinc in Alzheimer’s disease senile plaques. J Neurol Sci, 158: 47–52
Machlin L J. Bendich A.1987. Free radical tissue damage: protective role of antioxidant nutrients.FASEB J, 1:441-445
Malis C D,Bonventre J V.1986.Mechanism of calcium potentiation of oxygen free radical injury to renalmitochondria.A model for-post-ischemic and toxic mitochondrial damage.Biol Chem,261:14201-14208
Malmkvist J and Hansen S W. 2001.The welfare of farmed mink (Mustela vison) in relation to behavioural selection: A review. Animal Welfare,10: 41-52
Mancuso M. CoppedèF. Migliore L. Siciliano G. Murri L.2006.Mitochondrial dysfunction,oxidative stress and neurodegeneration, J Alzheimers Dis. 14:59-73
Marcus D L, Thomas C, Rodriguez C, Simberkoff K, Tsai J S, et al.1998. Increased peroxidation and reduced antioxidant enzyme activity in Alzheimer's disease. Experimental Neurology,150(1):40-44
Mason G J, Cooper C, Clarebrough C. 2001. The welfare of fur-farmed mink. Nature, 410:35-36
Mason G J. 1993.Age and context affect the stereotypies of caged mink. Behaviour, 127:191-229
Mason G J. 1995.Tail-biting in mink (Mustela vison) is influenced by age at removal from the mother. Animal Welfare, 3:305-311.
Mason GJ. 1991.Stereotypy: a critical review. Animal Behavior, 41: 1015–1038. Mason k E, Hartsouggh R. 1951.“Steatitis”or“yellow fat”in mink, and its relation to dietary fats and inadequacy of vitamin E. J Am Vet Med Assoc 119:72-75
Mason, G J. 1994.Tail-biting in mink (Mustela vison) is in?uenced by age at removal from the mother. Animal Welfare, 3(4), 305–311
Mason, G. J. 1992.Stereotypy and welfare in mink. J. Anim. Sci. 70:(suppl.1):158.
Mason, G. J. 1993.Age and context affect the stereotypies of caged mink. Behaviour, 127:191-229
Mason,G J. 1996.Early weaning enhances later development of stereotypy in mink. In: Duncan IJH, Widowski T, Haley DB (Eds). Proceedings of the 30th International Congress of the International Society for Applied Ethology:16
Mathews C A, Waller J, Glidden D, Lowe T L, Herrera L D, Budman C L, Erenberg G, Naarden A, Bruun R D, Freimer N B, Reus V I. 2004. Self injurious behaviour in Tourette syndrome: correlates with impulsivity and impulse control. Journal of Neurology, Neurosurgery and Psychiatry,75(8): 149-1155
Migliore L, Fontana I, Trippi F, Colognato R, CoppedèF, Tognoni G, Nucciarone B, Siciliano G. 2005. Oxidative DNA damage in peripheral leukocytes of mild cognitive impairment and AD patients. Neurobiol Aging, 26(5):567-73
Migliore, L. Fontana, I. Colognato, R. et al. 2005. Searching for the role and themost suitable biomarkersof oxidative stress in Alzheimer’s disease and in other neurodegenerative diseases. Neurobiol, 26:587–595 Mirella T,Marco G,Angelo C,et a1.2002.A P53一P66shc signaling pathway controls intracellular redox status.1evels of oxidation damaged DNA and oxidative stress induced apoptosis. Oncogene,21: 3872-3878
Morgan K, Tromborg C. 2007.Sources of stress in captivity. Applied Animal Behaviour Science, 102(3): 262-302
Mori, Tomohisa; Ito, Shinobu; Kita, Taizo; Narita, Minoru; Suzuki, Tsutomu; Matsubayashi, Kenji; Sawaguchi, Toshiko. 2007.Oxidative stress in methamphetamine-induced self-injurious behavior in mice. Behavioural Pharmacology, 18(3 ):239-249
Mueller K, Nyhan W L. 1980. Pharmacologic control of pemoline induced self-injurious behavior in rats. Pharmacol Biochem Behav,13(5):627-31
Mueller K, Hollingsworth E, Pettit H. 1986.Repeated pemoline produces self-injurious behavior in adult and weanling rats. Pharmacol Biochem Behav,25(5):933-938
Mueller K, Nyhan WL. 1982. Pharmacologic control of pemoline induced self-injurious behavior in rats. Pharmacol Biochem Behav,16(6):957-963
Mueller K, Saboda S, Palmour R, et al. 1998.Self-injurious behavior produced in rats by daily caffeine and continuous amphetamine.Dev Neurosci, 20(2/3):180-187
Nemmiche S, Chabane-Sari D, Guiraud P.2007. Role of alpha-tocopherol in cadmium-induced oxidative stress in Wistar rat's blood, liver and brain. Chemico-Biological Interactions ,170(3): 221-230
Ning Ke,Wang Zheng-Guo,Chen Chang Cai,Li Jinming,Zhu Peifang. 1999.Effects of excitatory amino acids and nimodipine on calcium currents in cultured rat cortical neurons.中国药理学报,20(4):329-333
Novgorodov S A,Gogvadze V G,Medvedeve B J,et,a1.1989. The effect of butylated hydr-oxytoluene,an inhibitor of lipid peroxidation on the calcium-induced uncoupling of rat liver mitochondria.FEBS Lett,248(1-2):179—181
Ookawara T, Matsuura N, Oh-ishi T, Okazaki M, Kizaki T, Suzuki K, Hitomi Y, Suzuki K, Ohno H. 2000. Serum extracellular superoxide dismutase in pediatric patients with various diseases as judged by an ELISA. Research Communications in Molecular Pathology & Pharmacology 107(3-4):291-296
Ozaki M ,Deshpande S S,Angkeow P,et a1 . 2000. Inhibition of the Racl GT-Pase protects against nonlethal ischrmitdreped'usion-induced necrosis and apoptosis in vivo.FASEB J,14:4l8-429
Pacifici R E, Davies K J. 1991.Protein, lipid and DNA repair systems in oxidative stress: the free-radical theory of aging revisited. Gerontology , 37(1-3):166-80.
Qureshi G A, Qureshi A A, Memon S A, Parvez S H.2006. Impact of selenium, iron,copper and zinc in on/off Parkinson’s patients on l-dopa therapy. J Neural Transm, Suppl. 71 :229–236
Qureshi, G A (Eds.). 2007.Oxidative Stress and Neurodegenerative Disorders. Elsevier Science Reinhardt V. 1994. Pair-housing rather than single-housing for laboratory rhesus macaques. Journal of Medical Primatology,23: 426-431
Rushen J P. 1985.Stereotypies aggression and the feeding schedules of tethered sows. Appl Anim Behav Sci,14: 137–147
Sahakian B J, Robbins T W, Morgan M J, Iversen S D.1975.The effects of psychomotor stimulants on stereotypy and locomotor activity in socially-deprived and control rats. Brain Research, 84: 195–205
Sallman H P, Drommer W, Solaro K L.1988. Pathogenic and metabolic impact on broilers strained by oxidized fats. Israel Journal of Veterinary Medicine,44(3):183-194
Sansom D, Krishnan V H, Corbett J, Kerr A.1993. Emotional and behavioural aspects of Rett syndrome,35(4): 340-345
Sara P D and Richard W J. 2004.Genetic and environmental factors modulating serum concentrations and activities of the antioxidant enzyme paraoxonase-1. Clinical Science , 107:435–447
Scherer N M, Deamer D W.1986. Oxidative stress impairs the function of sarcoplasmic reticulum by oxidation of sulfhydryl groups in the Ca2+-ATPase. Archives of Biochemistry and Biophysics,246(2):589–601
Schuessel K, Sch?fer S, Bayer T A, Czech C, Pradier L, Müller-Spahn F, Müller W E, Eckert A.2005. Impaired Cu/Zn-SOD activity contributes to increased oxidative damage in APP transgenic mice. Neurobiology of Disease,18(1):89-99
Suhail Kasim, H.A. Jinnah .2003.Self-Biting Induced by Activation of L-Type Calcium Channels in Mice: Dopaminergic Influences.Dev Neurosci, 25:20-25
Sheldon B W ,Curtis P A,Dawson P L,et a1.1997.Effect of dietary vitam in E on the oxidative stability,flavour,colour and volatile profiles of refrigerated and frozen turkey breast meat.Poultry Science,76:634—641
Shen H M, Shi C Y, Lee H P, Ong C N.1994. Aflatoxin B1-induced lipid peroxidation in rat liver. Toxicol. Appl. Pharmacol, 127: 145-150
Shibata, N. Kobayashi, M. 2008.The role for oxidative stress in neurodegenerative diseases. Brain Nerve, 60(2):157-70
Simeon D, Stanley B, Frances A et al.1992. Self-mutilation in personality disorders: psychological and biological correlates. Am J Psychiatry,149(2):221-226
Singh R,Kaur B,Kalina I, Popov T A, et al.2007. Effects of environmental air pollution on endogenous oxidative DNA damage in humans, Mutat Res,620:71–82
Skovgaard K, Jeppesen L L, Hansen C P B.1997. The effect of swimming water and cage size on the behaviour of ranch mink (Mustela vison). Scientifur ,(21): 253 - 260
Skulachev V P.1999. Mitochondrial physiology and pathology; concepts of programmed death of organelles, cells and organisms, Mol Aspects Med, 20:139–184
Slater T F, Cheeseman K H,Davies M J, et al.1987. Free radical mechanisms in relation to tissue injury. Proceedings of the Nutrition Society ,46:1-12
S?derstr?m S, Fredriksson A, Dencker L, et al.1995.The effect of mercury vapour on cholinergic neurons in the fetal brain: studies on the expression of nerve growth factor and its low-and high-affinity receptors.Brain research.Developmental brain research,85(1):96-108
Sofic E, Lange K W, Jellinger K, Riederer P.1992. Reduced and oxidized glutathione in the substantia nigra of patients with Parkinson's disease. Neuroscience Letters,142 (2): 128-30
Staci D, Kies and Darragh P. 1982. Self-injurious behaviour: a comparison of caffeine and pemoline models in rats. Pharmacol Biochem Behav, 16(6):957-63
Stringari J A K C,Nunes J L, Franco D, Bohrer S C, Garcia A L C,Dafre Milatovic D O, Souza J B T, Rocha M, Aschner M, Farina.2008.Prenatal methylmercury exposure hampes glutathione antioxidant system ontogenesis and causes long-lasting oxidative stress in the mouse brain. Toxicol ApplPharmacol,227 :147–154
Suhail Kasim H A, Jinnah.2003. Self-Biting induced by activation of L-Type calcium channels in mice: dopaminergic influences. Developmental Neuroscience, (25):20-25
Sun Y, Oberley L W and Li Y. 1988.A simple method for clinical assay of superoxide dismutase. Clinical Chemistry, 34(3):497–500
Thome J, Gsell W, R?sler M, Kornhuber J, Fr?lich L, Hashimoto E,et al.1997.Oxidative-stress associated parameters (lactoferrin, superoxide dismutases) in serum of patients with Alzheimer's disease. Life Sciences ,60(1):13-19
Tinsley N, Iqbal M, Pumford N R, et al.2010. Investigation of mitochondrial protein expression and oxidation in heart muscle in low and high feed efficient male broilers in a single genetic line1. Poult Sci,89:349-352
Traber M G, Atkinson J. 2007.Vitamin E .Antioxidant and nothing more. Free Radical Biology and Medicine,43(1): 4–15
Verhasselt V, Goldman M, Willems F.1998. Oxidative stress up-regulates IL-8 and TNF-alpha synthesis by human dendritic cells. European Journal of Immunology, 28(11): 3886-3890
Veronesi B.2004. Nanometer size diesel exhaust particles are selectively toxic to dopaminergic neurons: the role of microglia, phagocytosis, and NADPH oxidase, FASEB, 18 :1618–1620
Villalba R, Harrington C J.2000. Repetitive self-injurious behavior: a neuropsychiatric perspective and review of pharmacologic treatments. Semin Clin Neuropsychiatry ,5(4):215-226
Vinke C M, Eenkhoorn N C, Netto W J, Fermont P C J, Spruijt B M. 2002.Stereotypic behaviour and tail biting in farmed mink (Mustela Vison) in a new housing system. Animal Welfare,11(2): 231-245
Vinke C M, Vanden Bos R, Spruijt B M.2004. Anticipatory activity and stereotypical behaviour in American mink (Mustela vison) in three housing systems differing in the amount of enrichments. Applied Animal Behaviour Science,89 (1-2): 145-161
Visser J E, Smith D W, Moy S S, Breese G R, Friedmann T, Rothstein J D, Jinnah HA.2002.Oxidative stress and dopamine deficiency in a genetic mouse model of Lesch-Nyhan disease. Developmental Brain Research,133(2):127-39
Vojdani A, Bock K, Hirani A K.2008. Low natural killer cell cytotoxic activity in autism: the role of glutathion, IL-2 and IL-15. Journal of Neuroimmunology, 205(1–2):148–154
Wander R C, Du S, Ketchum S O, Rowe K E. 1996.α-Tocopherol influences in vivo indices of lipid peroxidation in postmenopausal women given fish oil. J Nutr, 126:643–652
Wang Z, Bunce G E, Hess J L. 1993.Selenite and Ca2+ homeostasis in the rat lens: effect on Ca-ATPase and passive Ca2+ transport. Current Eye Research ,12(3):213–218
Waschulewski I H , Sunde R A.1988. Effect of dietary methionine on tissue selenium and glutathione peroxidase (EC 1.11.1.9) activity in rats given selenomethionine. Br J Nutr, 60(1):57-68
Waschulewski I H,Sunde R A.1998. Effect of dietary methionine on utilization of tissue selenium from dietary selenomethionine for glutathione peroxidase in the rat. J Nutr, 1118(3):367-374
Wong-Ekkabut J, Xu Z, Triampo W, Tang I M, Tieleman D P, Monticelli L.2007. Effect of lipid peroxidation on the properties of lipid bilayers: a molecular dynamics study. Biophysical journal ,93(12):4225-4236
Wu G,Fang Y Z,Yang S,et a1.2004.Glutathione metabolism and its implications for hea1th.J Nutr,134(3):489-492
Xie J, Fan R, Meng Z.2007. Protein oxidation and DNA–protein crosslink induced by sulfur dioxide in lungs, livers, and hearts from mice, Inhal Toxicol,19: 759–765
Young J F,Stagsted J ,Jensen S K, Karlsson A H, et al.2003. Ascorbic acid, alpha-tocopherol, and oregano supplements reduce stress-induced deterioration of chicken meat quality. Poultry Science,82( 8): 1343-1351
Zaidi S M, Naheed Banu. 2004. Antioxidant potential of vitamins A, E and C in modulating oxidative stress in rat brain. Clinica Chimica Acta,340(1-2): 229–233
Zhang X Y, Zhou D F, Qi L Y, Chen S, Cao L Y, Chen D C, Xiu M H, Wang F, Wu G Y, Lu L, Kosten T A, Kosten T R.2009.Superoxide dismutase and cytokines in chronic patients with schizophrenia: association with psychopathology and response to antipsychotics. Psychopharmacology, 204(1): 177-184