苏丹红Ⅳ对大鳞副泥鳅和泥鳅的毒性研究
摘要
随着我国经济的不断发展，人们对食品质量的要求标准也在不断的提高。近年来食品安全问题越来越突出，由于苏丹红在食品添加上所引起的恐慌，使人们越来越关注人工合成染料这类非食用食品添加剂对人体的危害。因此，通过毒理学和分子生物学的原理方法来研究非法食品添加剂对动物的毒理学效应，以及动物食用后对动物遗传物质DNA损伤程度的研究，对于当前制定非食用添加剂的使用安全指标具有非常重要的理论和现实意义。
本研究根据评价外源物质毒性作用的毒理学标准，从急性毒性试验、生理毒性试验、遗传毒性试验(微核及核异常试验)、胚胎及仔鱼毒性试验、DNA损伤的RAPD分析五个方面初步探讨了苏丹红Ⅳ(Sudan Ⅳ)对两种泥鳅(大鳞副泥鳅和泥鳅)的毒性效用及DNA损伤效应。获得了如下结果：
1．急性毒性试验表明，苏丹红Ⅳ(Sudan Ⅳ)对大鳞副泥鳅的24h半数致死浓度(median lethal concentration，LC50)为2.125g.L~(-1)，48h半数致死浓度(median lethalconcentration，LC50)为1.925g.L~(-1)，安全浓度(safe concentration，Sc)为0.474g.L~(-1)；苏丹红Ⅳ (Sudan Ⅳ)对泥鳅的24h半数致死浓度为2.225g.L~(-1)，48h半数致死浓度为2.025g.L~(-1)，安全浓度为0.503g.L~(-1)。结果表明泥鳅相对于大鳞副泥鳅对苏丹红Ⅳ具有较高的耐受性。
2．在急性毒性试验结果的基础上，设置不同浓度梯度，进一步探讨了苏丹红Ⅳ对血细胞微核率及核异常率的影响。苏丹红Ⅳ (Sudan Ⅳ)对大鳞副泥鳅的设计染毒浓度分别为A(0.025g.L~(-1))、B(0.050g.L~(-1))、C(0.100g.L~(-1))、D(0.200g.L~(-1))、E(0.400g.L~(-1))以及空白对照组；苏丹红Ⅳ (Sudan Ⅳ)对泥鳅的设计染毒浓度分别为A(0.030g.L~(-1))、B(0.060g.L~(-1))、C(0.120g.L~(-1))、D(0.240g.L~(-1))、E(0.480g.L~(-1))以及空白对照组。染毒后1、2、3、4、5天分别取材，观察、计算微核率。结果显示，两种泥鳅红细胞微核率及核异常率与苏丹红Ⅳ浓度大体上呈正相关，同时也有一定的时间效应。
3．以两种泥鳅肝组织中谷丙转氨酶(GPT)、谷草转氨酶(GOT)的活性变化为指标，检测了苏丹红Ⅳ对两种泥鳅的生理毒性效用。实验数据显示受试动物肝脏GOT和GPT活性随着染毒时间的延长呈现出明显的波动，具体表现为先上升再下降最后一天又开始上升。这种特殊的现象也许表明不仅苏丹红Ⅳ本身能够影响泥鳅的生理功能，其次级代谢物对其生理功能也有明显的影响。
4．从50条10个碱基序列的随机引物中筛选出8条能产生较多扩增条带的随机引物，以染毒泥鳅和大鳞副泥鳅基因组DNA为模板，分析基因组DNA的RAPD分子标记谱带变化规律并与空白对照进行比较，进一步探究苏丹红Ⅳ对两种泥鳅基因组DNA的损伤情况。分析结果发现，在不同浓度不同时间染毒基因池中，苏丹红Ⅳ能不同程度地诱使RAPD谱带的增加、缺失以及带的亮度强弱的变化。结果表明苏丹红Ⅳ能够诱发基因组DNA的部分碱基发生突变。另外，本研究还对染毒后部分新产生的RAPD谱带进行了克隆测序和序列分析，这些研究结果对于揭示苏丹红毒性的分子机理具有重要的参考意义。
5．本研究还进一步分析了苏丹红Ⅳ对两种泥鳅胚胎和仔鱼发育分化的影响。以两种泥鳅的胚胎孵化率和畸形率为指标，在两种泥鳅受精卵发育至原肠胚中期时开始进行染毒，为开始处理时间进行染毒培养，探讨其对胚胎毒性效应。实验结果表明，苏丹红Ⅳ能不同程度地诱使两种泥鳅受精卵孵化率降低、畸形率升高，对胚胎发育致畸、致死作用明显。同时，两种泥鳅的胚胎对苏丹红Ⅳ的敏感程度也存在一定的差异。
以上结果表明，苏丹红Ⅳ对两种泥鳅的胚胎发育、抗氧化酶的活性、遗传物质的稳定性具有较明显的毒性作用，应当严格禁止其作为添加剂出现在食品中。
With the continuous growth of the national economy, people's food quality standards graduallyimprove. In recent years as Sudan red in food adds the panic, people pay more and more attention to thiskind of synthetic dyes non edible food additive which is harmful to the human body. Therefore, thestudy of toxicology and molecular biology principle method, used to study the toxic substances onanimal DNA injury severity, monitoring food toxic substance in action, has very important theoreticaland practical significance for the current formulation of additives in food safety in use indicator.
This study based on toxicological evaluation of exogenous substances toxic effects, is divided intofive parts: acute toxicity test, physiological toxicity test, genetic toxicity test (micronucleus test),embryonic and larval toxicity test, DNA injury: a RAPD analysis. We preliminary discussed the toxicityand molecular biological effects of Sudan red IV (Sudan IV) on two kinds of Loach (Misgurnusanguillicaudatus,). On the basis of the toxicology and molecular biology experimental results on SudanIV (Sudan IV) toxicity, make scientific assessment, providing digital basis for reasonable formulationof food in Sudan IV (Sudan IV) use safety indicators, in order to serve our country food safetyproduction better.
Through acute toxicity test, the Sudan red IV (Sudan IV) on Loach24h median lethal concentration(median lethal concentration, LC50)2.125g.L~(-1),48h median lethal concentration (median lethalconcentration, LC50)1.925g.L~(-1), safe concentration (safe concentration, Sc)0.474g.L~(-1); Sudan IV(Sudan IV) on the24h median lethal concentration (median lethal concentration, LC50)2.225g.L~(-1),48h median lethal concentration (median lethal concentration, LC50)2.025g.L~(-1), safe concentration(safe concentration, Sc)0.503g.L~(-1).
Based on the results of acute toxicity test, the genetic toxicity test (of micronuclei and nuclearanomalies test). With blood cell micronucleus rate as an index, designed each test group concentration.Sudan IV (Sudan IV) on Loach exposure concentrations were A (0.025g.L~(-1)), B (0.050g.L~(-1)), C(0.100g.L~(-1)), D (0.200g.L~(-1)), E (0.400g.L~(-1)),0(control group), a total of6groups; Sudan IV (Sudan IV) on Loach exposure concentrations were A (0.030g.L~(-1)), B (0.060g.L~(-1)), C (0.120g.L~(-1)),D (0.240g.L~(-1)), E (0.480g.L~(-1)),0(control group), divided into6groups. Processing time in exposureafter1,2,3,4, and5days respectively with a material, observation, calculation. The results showed,in two species of loaches erythrocyte micronucleus and abnormal nucleus and Sudan IV concentrationgenerally positively correlated, but also have a certain time effect.
According to the genetic toxicity test do the physiological toxicity test, with aminotransferase (GPT),aspartate aminotransferase (GOT) activity of the two kinds of Loach Liver alanine as indicator,.Experimental data shows the liver GOT and GPT activity increased with the prolongation of time, thenfall, however, on the last day, it began to rise again, descripting loach liver has the detoxificationfunction itself. As time goes on, the GOT and GPT activity will gradually periodicly changes. Theinhibition degree of the enzyme varies from one kind of loach to another.
In order to further explore the Sudan red IV (Sudan IV) in two species of loaches in the level of DNAdamage, screening8primers from50random primers, performed a RAPD (random amplifiedpolymorphic DNA) molecular markers on Loach, analysising the DNA damage of the two kinds ofloaches before and after the exposure. The analysis results show that, the Sudan red IV (Sudan IV) canto a different degree induce the addtion, deletion of the DNA fragment of the two species of loaches,and alteration of band brightness, obviously shown in the level of DNA damage effect.
At the embryo toxicity test, with two kinds of loach embryo hatching rate and abnormal rate asindexes, studied the toxicity effec of the Sudan red IV (Sudan IV) on the embryo of the two kinds ofloaches. When the loaches were in the embryo gastrulation period, they were exposed to medium forcultivation, experimental results show that, Sudan IV (Sudan IV) to different degrees can reduce twokinds of loaches embryo hatching rate, increase deformity rate, leading to teratogenic, lethal effecton the embryonic development level to some extent. The degree of sensitivity varies from one kind ofloach embryo to another.
本研究根据评价外源物质毒性作用的毒理学标准，从急性毒性试验、生理毒性试验、遗传毒性试验(微核及核异常试验)、胚胎及仔鱼毒性试验、DNA损伤的RAPD分析五个方面初步探讨了苏丹红Ⅳ(Sudan Ⅳ)对两种泥鳅(大鳞副泥鳅和泥鳅)的毒性效用及DNA损伤效应。获得了如下结果：
1．急性毒性试验表明，苏丹红Ⅳ(Sudan Ⅳ)对大鳞副泥鳅的24h半数致死浓度(median lethal concentration，LC50)为2.125g.L~(-1)，48h半数致死浓度(median lethalconcentration，LC50)为1.925g.L~(-1)，安全浓度(safe concentration，Sc)为0.474g.L~(-1)；苏丹红Ⅳ (Sudan Ⅳ)对泥鳅的24h半数致死浓度为2.225g.L~(-1)，48h半数致死浓度为2.025g.L~(-1)，安全浓度为0.503g.L~(-1)。结果表明泥鳅相对于大鳞副泥鳅对苏丹红Ⅳ具有较高的耐受性。
2．在急性毒性试验结果的基础上，设置不同浓度梯度，进一步探讨了苏丹红Ⅳ对血细胞微核率及核异常率的影响。苏丹红Ⅳ (Sudan Ⅳ)对大鳞副泥鳅的设计染毒浓度分别为A(0.025g.L~(-1))、B(0.050g.L~(-1))、C(0.100g.L~(-1))、D(0.200g.L~(-1))、E(0.400g.L~(-1))以及空白对照组；苏丹红Ⅳ (Sudan Ⅳ)对泥鳅的设计染毒浓度分别为A(0.030g.L~(-1))、B(0.060g.L~(-1))、C(0.120g.L~(-1))、D(0.240g.L~(-1))、E(0.480g.L~(-1))以及空白对照组。染毒后1、2、3、4、5天分别取材，观察、计算微核率。结果显示，两种泥鳅红细胞微核率及核异常率与苏丹红Ⅳ浓度大体上呈正相关，同时也有一定的时间效应。
3．以两种泥鳅肝组织中谷丙转氨酶(GPT)、谷草转氨酶(GOT)的活性变化为指标，检测了苏丹红Ⅳ对两种泥鳅的生理毒性效用。实验数据显示受试动物肝脏GOT和GPT活性随着染毒时间的延长呈现出明显的波动，具体表现为先上升再下降最后一天又开始上升。这种特殊的现象也许表明不仅苏丹红Ⅳ本身能够影响泥鳅的生理功能，其次级代谢物对其生理功能也有明显的影响。
4．从50条10个碱基序列的随机引物中筛选出8条能产生较多扩增条带的随机引物，以染毒泥鳅和大鳞副泥鳅基因组DNA为模板，分析基因组DNA的RAPD分子标记谱带变化规律并与空白对照进行比较，进一步探究苏丹红Ⅳ对两种泥鳅基因组DNA的损伤情况。分析结果发现，在不同浓度不同时间染毒基因池中，苏丹红Ⅳ能不同程度地诱使RAPD谱带的增加、缺失以及带的亮度强弱的变化。结果表明苏丹红Ⅳ能够诱发基因组DNA的部分碱基发生突变。另外，本研究还对染毒后部分新产生的RAPD谱带进行了克隆测序和序列分析，这些研究结果对于揭示苏丹红毒性的分子机理具有重要的参考意义。
5．本研究还进一步分析了苏丹红Ⅳ对两种泥鳅胚胎和仔鱼发育分化的影响。以两种泥鳅的胚胎孵化率和畸形率为指标，在两种泥鳅受精卵发育至原肠胚中期时开始进行染毒，为开始处理时间进行染毒培养，探讨其对胚胎毒性效应。实验结果表明，苏丹红Ⅳ能不同程度地诱使两种泥鳅受精卵孵化率降低、畸形率升高，对胚胎发育致畸、致死作用明显。同时，两种泥鳅的胚胎对苏丹红Ⅳ的敏感程度也存在一定的差异。
以上结果表明，苏丹红Ⅳ对两种泥鳅的胚胎发育、抗氧化酶的活性、遗传物质的稳定性具有较明显的毒性作用，应当严格禁止其作为添加剂出现在食品中。
With the continuous growth of the national economy, people's food quality standards graduallyimprove. In recent years as Sudan red in food adds the panic, people pay more and more attention to thiskind of synthetic dyes non edible food additive which is harmful to the human body. Therefore, thestudy of toxicology and molecular biology principle method, used to study the toxic substances onanimal DNA injury severity, monitoring food toxic substance in action, has very important theoreticaland practical significance for the current formulation of additives in food safety in use indicator.
This study based on toxicological evaluation of exogenous substances toxic effects, is divided intofive parts: acute toxicity test, physiological toxicity test, genetic toxicity test (micronucleus test),embryonic and larval toxicity test, DNA injury: a RAPD analysis. We preliminary discussed the toxicityand molecular biological effects of Sudan red IV (Sudan IV) on two kinds of Loach (Misgurnusanguillicaudatus,). On the basis of the toxicology and molecular biology experimental results on SudanIV (Sudan IV) toxicity, make scientific assessment, providing digital basis for reasonable formulationof food in Sudan IV (Sudan IV) use safety indicators, in order to serve our country food safetyproduction better.
Through acute toxicity test, the Sudan red IV (Sudan IV) on Loach24h median lethal concentration(median lethal concentration, LC50)2.125g.L~(-1),48h median lethal concentration (median lethalconcentration, LC50)1.925g.L~(-1), safe concentration (safe concentration, Sc)0.474g.L~(-1); Sudan IV(Sudan IV) on the24h median lethal concentration (median lethal concentration, LC50)2.225g.L~(-1),48h median lethal concentration (median lethal concentration, LC50)2.025g.L~(-1), safe concentration(safe concentration, Sc)0.503g.L~(-1).
Based on the results of acute toxicity test, the genetic toxicity test (of micronuclei and nuclearanomalies test). With blood cell micronucleus rate as an index, designed each test group concentration.Sudan IV (Sudan IV) on Loach exposure concentrations were A (0.025g.L~(-1)), B (0.050g.L~(-1)), C(0.100g.L~(-1)), D (0.200g.L~(-1)), E (0.400g.L~(-1)),0(control group), a total of6groups; Sudan IV (Sudan IV) on Loach exposure concentrations were A (0.030g.L~(-1)), B (0.060g.L~(-1)), C (0.120g.L~(-1)),D (0.240g.L~(-1)), E (0.480g.L~(-1)),0(control group), divided into6groups. Processing time in exposureafter1,2,3,4, and5days respectively with a material, observation, calculation. The results showed,in two species of loaches erythrocyte micronucleus and abnormal nucleus and Sudan IV concentrationgenerally positively correlated, but also have a certain time effect.
According to the genetic toxicity test do the physiological toxicity test, with aminotransferase (GPT),aspartate aminotransferase (GOT) activity of the two kinds of Loach Liver alanine as indicator,.Experimental data shows the liver GOT and GPT activity increased with the prolongation of time, thenfall, however, on the last day, it began to rise again, descripting loach liver has the detoxificationfunction itself. As time goes on, the GOT and GPT activity will gradually periodicly changes. Theinhibition degree of the enzyme varies from one kind of loach to another.
In order to further explore the Sudan red IV (Sudan IV) in two species of loaches in the level of DNAdamage, screening8primers from50random primers, performed a RAPD (random amplifiedpolymorphic DNA) molecular markers on Loach, analysising the DNA damage of the two kinds ofloaches before and after the exposure. The analysis results show that, the Sudan red IV (Sudan IV) canto a different degree induce the addtion, deletion of the DNA fragment of the two species of loaches,and alteration of band brightness, obviously shown in the level of DNA damage effect.
At the embryo toxicity test, with two kinds of loach embryo hatching rate and abnormal rate asindexes, studied the toxicity effec of the Sudan red IV (Sudan IV) on the embryo of the two kinds ofloaches. When the loaches were in the embryo gastrulation period, they were exposed to medium forcultivation, experimental results show that, Sudan IV (Sudan IV) to different degrees can reduce twokinds of loaches embryo hatching rate, increase deformity rate, leading to teratogenic, lethal effecton the embryonic development level to some extent. The degree of sensitivity varies from one kind ofloach embryo to another.
引文
[1]李龙川.非食用食品添加剂苏丹红的危害及其主要检测方法[J].商情，2009，32(2):13-13.
[2] Vijayavel K., Balasubramanianm P.. Fluctuations of biochemi2cal const ituents and marker enzymesas a consequence of naphthalene toxicity in the edible estuarine crab Scylla serrata [J]. Ecotoxi colEnvi ron Saf,2006,63(1):1412-1471
[3]卫生部.苏丹红危险性评估报告[J].中国食品卫生杂志,2005,17(5):276—278
[4] Lin L., Zengx L., Zhang J.. Effect of profenofos poisoning on liver lipid peroxidat ion and liver function in rabbits [J]. Chinese J ournal of Clinic Rehabi litation,2004,8(21):43802-43811
[5]刘丽娜,林天乐,曹永.偶氮染料-苏丹红[J].精细与专用化学品,2005,13(8):16-17.
[6]国家质量监督检验检疫总局. GB/PT19681—2005食品中苏丹红染料的检测方法[s].北京:中国标准出版社,2005
[7]潘志明,李忠,王冰等.食品中苏丹红检测研究进展[J].世界科技研究与发展.2007.12(6):14-18
[8]谢斌,丁玉峰.毒理学的研究进展[J]. Herald of Medicine,2007,10(26):1186-1187.
[9]吴浩,袁伯俊.毒理学新技术与发展趋势[J].中国新药杂志,2000,9(6):367-370.
[10]顾祖维.我国毒理学的发展与展望[J].上海预防医学杂志,2004.16(6):253-255.
[11]乔赐彬.毒理学的发展与期望[J].职业与健康,2004,20(6):1-4.
[12]张天宝.毒理学的挑战、机遇个发展趋势[J].卫生毒理学杂志,2003,17(1):2-5.
[13]肖凯,李宏霞.遗传毒性试验方法应用现况与研究进展[J].现代预防医学,2004,31(4):524-526.
[14]李寿祺.毒理学原理方法(第二版)[M].成都:四川大学出版社,2003,153-177.
[15] Liu H. L., Yu H. X., Xu T. L. et al.2005. Effects of Benzidine congenerson two am inopherases ingold fish liver [J]. Journal of Agro2Environment Science,24(6):1069—1074(in Chinese)
[16] Mannag K., Banerjee G., Gupta S. Micronucleus test in the periperel erythrocytes of the exotic fish.Oreochrcm is mossam bica[J]. The Nucleus,1985,28(3):176-179.
[17] Arkhipchuk V., Garanko N. Using the nucleolar biomarker and the micronucleus test on in vivo fishfin cells[J]. Ecotoxicology and Environmental Safety,2005,62(1):42-52.
[18]夏元询.化学物质毒性全书[M].上海:上海科学技术文献出版社,1991:720.
[19]印木泉.遗传毒理学[M]. Beijing: Academic Press,2002,414.
[20]邢卫平,赵恒奎,姜宗荣.微核及微核试验在遗传毒理学中的应用[J].安徽预防医学杂志2002,8(5):317—320.
[21] Stich H. F., San R. H., Rosin M. P.. Adaptation of the DNA-repair and micronucleus tests to humancell suspensions and exfoliated cells[J]. Acadme. Science.,1983,407:93–105.
[22] Rosin M. P., Anwar W. Chromosomal damage in urothelial cells from Egyptians with chronicSchistosoma haematobium infections[J]. Cancer,1992,50:539–543.
[23] Heddle J. A., Cimino M. C., Hayash L M., et al.. Micronuclei as an index of cytogenetic damage:Past, Present and Future[J]. Environment. Molecular Mutagen,1991,18:277–291.
[24] Suruda A., Schulte P., Boeniger M., et al.. Cytogenetic effects of formaldehyde exposure instudents of mortuary science[J]. Cancer Epidemiol. Biomarkers Prevent,1993,2:453–460.
[25] Holland, N. T. Levine A. J., Smith M. T., et al.. Quantification of epithelial cell micronuclei byfluorescence in situ hybridization (FISH) in mortuary science students exposed to formaldehyde[J].Mutational Research,1996,371:237–248.
[26] Sandra P., Guillamon M., Barcelo D.. Quantitative analysis of polycyclicaromatic hydrocarbons insewage sludge from wastewater treatment plants[J]. Journal of hromatography,2001,938(59):57-65.
[27]谢志浩,蔡亚非,陈国等.四种除草剂对泥鳅红细胞微核及核异常诱导[J].水产科学,2004,23(6):17-19.
[28]陈军建,夏宜琤.青蛙蝌蚪微核试验------一种水体诱变剂检测系统的建立[J].水生生物学报,1993,17(4):298–308.
[29]钱晓薇.乙酸铜对黄鳝红细胞微核及核异常的影响[J].江西科学,2004,22(5):331–333.
[30]楼允东,吴萍.1996.亚硝基胍对泥鳅红细胞微核及核异常的诱发[J].中国环境科学,16(4):275—278.
[31]耿龙武,蔺玉华,王海涛,等.2003.铬对鲤嗜多染红细胞微核的诱变效应[J].水产学杂志,16(2):63—67.
[32]向德标.敌敌畏对泥鳅红细胞核的诱变效应[J].烟台师范学院学报:自然科学版,1999,15(2):134-137.
[33]薛良义.三种农药对黄鳝红细胞微核的诱导[J].浙江水产学院学报,1993,12(3):174-179.
[34] Atienzar, F. A., Jha, A. N.,2006. The random amplified polymorphic DNA (RAPD) assay andrelated techniques applied to genotoxicity and carcinogenesis studies: a critical review. Mutat. Res.613,76–102.
[35] Atienzar, F. A., Jha, A. N.,2004. The random amplified polymorphic DNA (RAPD) assay todetermine DNA alterations, repair and transgenerational effects in B[a]P exposed Daphnia magna.Mutat. Res.552,125–140.
[36] Atienzar, F. A., Billinghurst, Z., Depledge, M. H.,2002.4-n-Nonylphenol and17-beta estradiolmay induce common DNA effects in developing barnacle larvae. Environ. Pollut.120,735–738.
[37] Atienzar, F. A., Cordi, B., Donkin, M. E., Evenden, A. J., Jha, A. N., Depledge, M. H.,2000.Comparison of ultraviolet-induced genotoxicity detected by random amplified polymorphic DNAwith chlorophyll fluorescence and growth in a marine macroalgae Palmaria palmata. Aquat. Toxicol.50,1–12.
[38] Becerril, C., Ferrero, M., Sanz, F., Castano, A.,1999a. Detection of mitomycin C-induced geneticdamage in fish cells by use of RAPD. Mutagenesis14(5),449–456.
[39] Bau, D. T., Wang, T. S., Chung, C. H., Wang, A. S., Wang, A. S., Jan, K. Y.,2002. Oxidative DNAadducts and DNA–protein cross-links are the major DNA lesions induced by arsenite. Environ.Health Perspect.110(Suppl.5),753–756.
[40] Becerril, C., Ferrero, M., Sanz, F., Castano, A.,1999b. Detection of mitomycin C-induced geneticdamage in fish cells by use of RAPD. Mutagenesis14,449–456.
[41] Castano, A., Becerril, C.,2004. In vitro assessment of DNA damage after short-and long-termexposure to benzo[a]pyrene usingRAPD and the RTG-2fish cell line. Mutat. Res.552,141–151.
[42] F. A. Atienzar, A. N. Jha, The random amplified polymorphic DNA (RAPD) assay to determine DNAalterations, repair and transgenerational effects in B(a)P exposed Daphnia magna, Mutat. Res.552(2004)125–140.
[43] I. I. Ploskonosiva, V. I. Baranov, A. I. Gaziev, PCR assay of DNA damage and repair at the gene levelin brain and spleen of gamma irradiated young and old rats, Mutat. Res.434(1999)109–117.
[44] C. Quintela-Sabaris, P. S. Kidd, M. I. Fraga, Identification of metal liferous ecotypes of Cistusladanifer L. using RAPD markers, Z. Naturforsch.60(2005)229–235.
[45] C. Conte, I. Mutti, P. Puglisi, DNA fingerprinting analysis by a PCR based method for monitoring thegenotoxic effects of heavy metals pollution, Chemosphere37(1998)2739–2749.
[46] M. R. Enan, Application of randomamplified polymorphicDNA (RAPD) to detect the genotoxiceffect of heavy metals, Biotechnol. Appl. Biochem.43(2006)147–154.
[47] D. H. Blust, T. Backeljau, The population genetic structure of Littorina littorea (Mollusca:Gastropoda) along a pollution gradient in the Scheldt estuary (The Netherlands) using RAPDanalysis, Sci. Total. Environ.325(2004)59–66.
[48] Wan Liua, Y. S. Yangb, c,*, P. J. Li a, Q. X. Zhoua, L. J. Xiea, Y. P. Hana, Risk assessment ofcadmium-contaminated soil on plant DNA damage using RAPD and physiological indices, Journal ofHazardous Materials161(2009)878–883.
[49] Yuan-Cho Lee a, Vivian. C. Yang a, Tsu-Shing Wang b,*, Use of RAPD to detect sodiumarsenite-induced DNA damage in human lymphoblastoid cells, Toxicology239(2007)108–115.
[50]郑永华,蒲富永.汞对鲤鲫鱼组织转氨酶活性的影响[J].西南农业大学学报,1997,19(1):41-45.
[51]贾秀伟,陈志伟.镉对鲫鱼组织转氨酶和过氧化氢酶活性的影响[J].环境污染与防止,1997,19(6):4-7.
[52]陈玉春,顾雪飞,刘敏.5种中草药对鲤血清谷丙转氨酶、谷草转氨酶及红细胞过氧化氢酶活性的影响[J].淡水渔业,2007,37(5):11-13.
[53]陈鹏飞,杨德强,邹红.两种中草药组方对鲫鱼肝脏转氨酶的影响[J].饲料工业,2005,(6):28-31.
[54]张晓红,张虎芳..胭脂红对泥鳅红细胞微核的形成和核异常的影响[J].中国西部科技,2006,3(1):26-28.
[55] Chen Jianjun, Cao Xianglin, Du Qiyan, et al.. Physiological toxicity and genotoxicity of Xingxiangwastewater on loach[J]. Environmental Pollution&Control,2008,30(11):31-34.
[56]张彬彬.乙草胺对泥鳅肝脏谷丙转氨酶和谷草转氨酶的影响[J].江苏农业科学,2009,1:289-290.
[57] LI Yun, RU Shaoguo. Effects of monocrotophos on GPT and GOT activities in the goldfish(Carassius auratus) livers and serum [J]. Journal of Safety and Environment,2008,8(5):9-12.
[58]冯健,刘永坚,田丽霞,等.草鱼实验性镉中毒的肝、肾病理学研究[J].中山大学学报(自然科学版),2003,42(2):226-230.
[59]郑永华,蒲富永.汞对鲤鲫鱼组织转氨酶活性的影响[J].西南农业大学学报,1997,19(1):4l-45.
[60]惠天朝,施明华,朱荫媚.硒对罗非鱼慢性镉中毒肝抗氧化酶及转氨酶的影响[J].中国兽医学报,2000,20(3):264-266.
[61] Chen Jianjun, Cao Xianglin, Du Qiyan, et al.. Physiological toxicity and genotoxicity of Xingxiangwastewater on loach[J]. Environmental Pollution&Control,2008,30(11):31-34.
[62]张彬彬.乙草胺对泥鳅肝脏谷丙转氨酶和谷草转氨酶的影响[J].江苏农业科学,2009,1:289-290.
[63] LI Yun, R. U. Shaoguo. Effects of monocrotophos on GPT and GOT activities in the goldfish(Carassius auratus) livers and serum [J]. Journal of Safety and Environment,2008,8(5):9-12.
[64]王丙莲,张迎梅,侯亚妮,等.镉铅对泥鳅组织转氨酶活性的影响[J].兰州大学学报(自然科学版),2006,4(3):67-70.
[65] Vaglio A., Landriscina C.. Change in liver Enzyme Activity in theTeleost Sparus aurata inResponse to Cadmium Intoxication[J]. Ecotoxicology and Environmental Safety,1999,43:111-116.
[66]徐维娜,谢国驷,刘文斌,等.敌百虫胁迫对异育银鲫鱼体中4种酶活性变化的影响[J].环境科学学报,2008,28(6):1198-1205.
[67]孔力,阎晓红,丁波.金双歧制剂中三种菌苗对大鼠血清GOT、GPT、γ-GT酶活性的影响[J].中国微生态学杂志[J].2000,12(3):183-184.
[68]刘伟,支兵杰,战培荣,等.盐度对大麻哈鱼幼鱼血液生化指标及肝组织的影响[J].应用生态学报,2010,21(9):2411-2417.
[69]刘存歧,刘丽静,王军霞,等.盐碱地渗水钙镁离子对凡纳滨对虾酶活力的影响[J].动物学杂志,2007,42(2):129-133.
[70]王虹扬,黄沈发,徐镜波,等.热污染对金鲫鱼组织内四种酶活性的影响[J].中国环境科学,2006,26(3):372-375.
[71]陈晨,黄峰,舒秋艳,等.共轭亚油酸对草鱼生长、肌肉成分、谷草转氨酶及谷丙转氨酶活性的影响[J].水生生物学报,2010,34(3):647-651.
[72]姚纪花,周平凡.铜、锌和甲胺磷对大鳞副泥鳅胚胎发育和仔鱼成活的影响[J].上海水产大学学报,1997,(1):11-16.
[73] Mckim, J. M.. Evaluation of tests with early life stage of fish for predicting long-term toxicity[J].Fish Ees. Board Can.,1977,34:1148-1154..
[74]贾秀英.镉对泥鳅幼鱼的急性和亚急性毒性研究[J].环境污染与防治,2001,23(5):227-228.
[75] LI Yang, WANG Weimin. Toxicity and Teratogenic Effects of Busulfan in Early DevelopingEmbryo and Larva of Zebrafish (Danio Rerio)[J]. Ecological Science,2008,27(5):368-375.
[76]周立红,陈学豪.四种重金属对泥鳅胚胎和仔鱼毒性的研究[J].厦门水产学院学报,1994,16(1):11-19.
[77]崔可译.汞等六种重金属对鱼卵孵化和仔鱼成活的影响[J].海洋与湖沼,1987,18(2):138-143.
[78] Rice, D. W., Harrison, F. L., and Jearld. A. Jr. Effects of copper of early life history stages ofnorthern anchovy EnCraulis mordax. Fishery Bulletin[J].1980,78(3):675-682.
[79]何斌,何利君,杜军,等.4种重金属离子对淡水石斑胚胎及仔鱼急性毒性的研究[J].水利渔业,2006,24(4):94-95,105.
[80]杨鸢劼.鱼类作为实验动物在环境毒理学研究中的应用[J].水产科技情报,2010,37(4):187-190
[81]陈朝阳,许淼清,谢进金.两种农药对金鱼的急性毒性研究[J].泉州师范学院学报(自然科学),2005,23(6):78-81.
[82]张娜.鱼类急性毒性实验及其条件选择[J].水利渔业,1999,19(6):65-68.
[83]王爱华,苏丹红Ⅰ对小鼠血液和脏器系数的影响,食品科学2010, Vol.31, No.05279,中图分类号: S851.4文献标识码: A文章编号:1002-6630(2010)05-0279-04.
[84] Stiborova M., Frei E., Schmeiger H. H.. Detoxi canon products of the carcinogenic azodye SudanI(Solvent Yellow14) bind to nucleic acids after activation by peroxidase[J]. Cancar Lett,1993,68:43-47.
[85] Stiborova M., Schmeiser H. H., Frei E.. Prostaglandin H synthase medicated oxidation and bindingto DNA of a detoxication metabol i te of carcinogenic Sudan I,1-(phenylazo)-2,6-dihydroxynaphthalene[J]. Cancer Lett,1999,146:53-60.
[86] Stiborovan M., Martinek V., Rydlova H., et al. Expression of cytochrome P4501A1and itscontribution to oxidation of a potential human carcinogen1phenylazo2naphthol(Sudan Ⅰ)inhuman livers[J]. Cancer Letters,2005,220:145-155.
[87]郎朗,于蕾,邹翔.苏丹红I, III, IV致小鼠氧化损伤的实验研究[J].哈尔滨商业大学学报:自然科学版,2005,21(6):687-689.
[88]安玉.苏丹红I号对HepG2细胞的遗传毒性及氧化性DNA损伤[D].大连医科大学,2007.
[89] Holland, N. T. Levine A. J., Smith M. T., et al.. Quantification of epithelial cell micronuclei byfluorescence in situ hybridization (FISH) in mortuary science students exposed to formaldehyde[J].Mutational Research,1996,371:237–248.
[90] Sandra P., Guillamon M., Barcelod D.. Quantitative analysis of polycyclicaromatic hydrocarbons insewage sludge from wastewater treatment plants[J]. Journal of hromatography,2001,938(59):57-65.
[91]郑琰晶,陈琳,陈燕平.十二烷基硫酸钠对水生生物的急性毒性影响[J].农业环境科学学报,2006,25(supl.):496-498.；
[92]杜启艳,吴小华,南平,常重杰。苏丹红Ⅰ对泥鳅红细胞微核率和组织磷酸酶活性的影响[J].安徽农业科学,2008,14:5902-5903
[93] Fischer B, Die experimentelle Erzeugung atypischer Epithelwucherungen unddie Entstehungbosartiger Geschwulste. Med Wochenschr,1906,53:2041
[94]徐厚恩,张铣.卫生毒理学基础[M].北京:北京医科大学中国协和医科大学联合出版社,1991:152-155.
[95]陈怀宇,谢进金,尤晓霞,等.汞对金鱼的急性毒性研究[J].泉州师范学院学报(自然科学),2007,25(6):107-110.
[96]聂晶磊,刘锋,周春玉,等.氯酚类化合物对金鱼的急性和亚急性毒性研究[J].环境科学研究,2001,14(3):6-8.
[97]瞿建国.锌对金鱼的急性毒性及体内的积累和分布[J].上海环境科学,1996,15(6):42—43.
[98]黄周英,谢进金,陈琳钦,等.敌敌畏对金鱼的急性毒性研究[J].毒理学杂志,2005,19(4):311-312.
[99] Guo Fenghong, WANG Zhi-he, CHEN Biwen, et al.. Acute Toxicity of Ammonia and Nitrite toAdult Siniperca chuatsi[J]. Food Science,2009,30(23):397-400.
[100] Hu Xiuzhi, ZHOU Chunjing, WU Ya, et al.. Acute Toxicity Study of Lead and Copper onCarassius auratus[J]. Journal of Neijiang Normal University,2009.24(12):45-48.
[101] Jiang Gangcheng. Study on the Acute Toxicity and Genetics Toxicity of Bensulfuron-methyl onDanio rerio[J]. Journal of Anhui Agricultural Sciences,2009,37(32):15879-15881.
[102] Yang Weidong, SHANG Wen, LIU Jiesheng. Acute Toxicities of Phaeocystis globosa on FiveAquatic Animals[J]. Journal of Tropical and Subtropical Botany,2009,17(1):68-73.
[103]姚纪花,周平凡.铜、锌和甲胺磷对大鳞副泥鳅胚胎发育和仔鱼成活的影响[J].上海水产大学学报,1997,(1):11-16.
[104]李莉,李效宇,孔祥会,等.金鱼胚胎发育的观察研究[J].河南水产,1996,3:24-25.
[105]张毓琪,陈叙龙.环境生物毒理学[M].天津:天津大学出版社,1993,257-258.
[106]惠秀娟.环境毒理学[M].北京:化学工业出版社,2003,270-271.
[107]杜荣骞.生物统计学[M].施普林格出版社,1997.
[108]胡庚东,陈家长,吴伟,等.除草剂丁草胺对黄鳝的遗传毒性[J].湛江海洋大学学报,2005,25(1):43-46.
[109]耿德贵,张大生,程伟,等.四种除草剂对中华大蟾蜍蝌蚪红细胞微核及核异常的影响[J].动物学杂志,2000,35(1):12–16.
[110]周静.离子液体对黑斑蛙胚胎及蝌蚪与隆肛蛙蝌蚪毒性的研究[D].新乡:河南师范大学,2007.
[111]朱毅,张永江.镉、铬、铜及其协同作用对鲤鱼嗜多染红细胞微核的诱发效应[J].南京师大学报(自然科学报),1999,22(3):60-63.
[112] Biggs M. L., Kalman D. A., Moore L. E., et al.. Relationship of urinary arsenium to intakeestimates and a biomarker of effect bladder cell micronucler[J]. Mut Res,1997,386(3):185-195.
[113] Sandra A., Miniss I.. Micronucleus test in erythrocytes of Barbus plebeius(Teleostei Pisces)fromtwo natural envirbarbrments a bioassay for the in situ detection ofmutagens in fresh water[J].Mutation Research/Genetic Toxicology,1996,367(4):245-251.
[114] Mulkiewicz E., JastorffF B., Sk A. C., et al.. Evaluation of the acute toxicity of per fluorinatedcarboxylic acids using eukaryotic cell lines bacteria and enzymatic assays[J]. EnvironmentalToxicology and Phamacologys,2007,23(3):279-285.
[115] Elhajouji A., Cunha M., Kirsch V. M., et al.. Spindle poisons can induce poiyploidy by mitoticslippage and micronucleates in the cytokinesisblock assay[J]. Mutagenesis,1998,13(2):193-198.
[116]汤新慧.除草剂诱发蟾蜍蝌蚪红细胞微核的研究[J].中国环境科学,1998,18(2):162-165.
[117] Lin L, Zeng X L, Zhang J. Effect of profenofos poisoning on liver lipid peroxidation and Liverfunction in rabbits[J]. Clinical Rehabilitation of China,2004,8(21):4380-4381.
[118]王丙莲,张迎梅,侯亚妮,等.镉铅对泥鳅组织转氨酶活性的影响[J].兰州大学学报(自然科学版),2006,4(3):67-70.
[119] Palanivelu V., Vijayavel K., Balasubramanian S. E.. Influence of insecticidal derivative (CartapHydrochloride)from the marinepolychaete on certain enzyme systems of the freshwater fishOreochromis mossambicus[J]. Environ Biol,2005,262:191-195.
[2] Vijayavel K., Balasubramanianm P.. Fluctuations of biochemi2cal const ituents and marker enzymesas a consequence of naphthalene toxicity in the edible estuarine crab Scylla serrata [J]. Ecotoxi colEnvi ron Saf,2006,63(1):1412-1471
[3]卫生部.苏丹红危险性评估报告[J].中国食品卫生杂志,2005,17(5):276—278
[4] Lin L., Zengx L., Zhang J.. Effect of profenofos poisoning on liver lipid peroxidat ion and liver function in rabbits [J]. Chinese J ournal of Clinic Rehabi litation,2004,8(21):43802-43811
[5]刘丽娜,林天乐,曹永.偶氮染料-苏丹红[J].精细与专用化学品,2005,13(8):16-17.
[6]国家质量监督检验检疫总局. GB/PT19681—2005食品中苏丹红染料的检测方法[s].北京:中国标准出版社,2005
[7]潘志明,李忠,王冰等.食品中苏丹红检测研究进展[J].世界科技研究与发展.2007.12(6):14-18
[8]谢斌,丁玉峰.毒理学的研究进展[J]. Herald of Medicine,2007,10(26):1186-1187.
[9]吴浩,袁伯俊.毒理学新技术与发展趋势[J].中国新药杂志,2000,9(6):367-370.
[10]顾祖维.我国毒理学的发展与展望[J].上海预防医学杂志,2004.16(6):253-255.
[11]乔赐彬.毒理学的发展与期望[J].职业与健康,2004,20(6):1-4.
[12]张天宝.毒理学的挑战、机遇个发展趋势[J].卫生毒理学杂志,2003,17(1):2-5.
[13]肖凯,李宏霞.遗传毒性试验方法应用现况与研究进展[J].现代预防医学,2004,31(4):524-526.
[14]李寿祺.毒理学原理方法(第二版)[M].成都:四川大学出版社,2003,153-177.
[15] Liu H. L., Yu H. X., Xu T. L. et al.2005. Effects of Benzidine congenerson two am inopherases ingold fish liver [J]. Journal of Agro2Environment Science,24(6):1069—1074(in Chinese)
[16] Mannag K., Banerjee G., Gupta S. Micronucleus test in the periperel erythrocytes of the exotic fish.Oreochrcm is mossam bica[J]. The Nucleus,1985,28(3):176-179.
[17] Arkhipchuk V., Garanko N. Using the nucleolar biomarker and the micronucleus test on in vivo fishfin cells[J]. Ecotoxicology and Environmental Safety,2005,62(1):42-52.
[18]夏元询.化学物质毒性全书[M].上海:上海科学技术文献出版社,1991:720.
[19]印木泉.遗传毒理学[M]. Beijing: Academic Press,2002,414.
[20]邢卫平,赵恒奎,姜宗荣.微核及微核试验在遗传毒理学中的应用[J].安徽预防医学杂志2002,8(5):317—320.
[21] Stich H. F., San R. H., Rosin M. P.. Adaptation of the DNA-repair and micronucleus tests to humancell suspensions and exfoliated cells[J]. Acadme. Science.,1983,407:93–105.
[22] Rosin M. P., Anwar W. Chromosomal damage in urothelial cells from Egyptians with chronicSchistosoma haematobium infections[J]. Cancer,1992,50:539–543.
[23] Heddle J. A., Cimino M. C., Hayash L M., et al.. Micronuclei as an index of cytogenetic damage:Past, Present and Future[J]. Environment. Molecular Mutagen,1991,18:277–291.
[24] Suruda A., Schulte P., Boeniger M., et al.. Cytogenetic effects of formaldehyde exposure instudents of mortuary science[J]. Cancer Epidemiol. Biomarkers Prevent,1993,2:453–460.
[25] Holland, N. T. Levine A. J., Smith M. T., et al.. Quantification of epithelial cell micronuclei byfluorescence in situ hybridization (FISH) in mortuary science students exposed to formaldehyde[J].Mutational Research,1996,371:237–248.
[26] Sandra P., Guillamon M., Barcelo D.. Quantitative analysis of polycyclicaromatic hydrocarbons insewage sludge from wastewater treatment plants[J]. Journal of hromatography,2001,938(59):57-65.
[27]谢志浩,蔡亚非,陈国等.四种除草剂对泥鳅红细胞微核及核异常诱导[J].水产科学,2004,23(6):17-19.
[28]陈军建,夏宜琤.青蛙蝌蚪微核试验------一种水体诱变剂检测系统的建立[J].水生生物学报,1993,17(4):298–308.
[29]钱晓薇.乙酸铜对黄鳝红细胞微核及核异常的影响[J].江西科学,2004,22(5):331–333.
[30]楼允东,吴萍.1996.亚硝基胍对泥鳅红细胞微核及核异常的诱发[J].中国环境科学,16(4):275—278.
[31]耿龙武,蔺玉华,王海涛,等.2003.铬对鲤嗜多染红细胞微核的诱变效应[J].水产学杂志,16(2):63—67.
[32]向德标.敌敌畏对泥鳅红细胞核的诱变效应[J].烟台师范学院学报:自然科学版,1999,15(2):134-137.
[33]薛良义.三种农药对黄鳝红细胞微核的诱导[J].浙江水产学院学报,1993,12(3):174-179.
[34] Atienzar, F. A., Jha, A. N.,2006. The random amplified polymorphic DNA (RAPD) assay andrelated techniques applied to genotoxicity and carcinogenesis studies: a critical review. Mutat. Res.613,76–102.
[35] Atienzar, F. A., Jha, A. N.,2004. The random amplified polymorphic DNA (RAPD) assay todetermine DNA alterations, repair and transgenerational effects in B[a]P exposed Daphnia magna.Mutat. Res.552,125–140.
[36] Atienzar, F. A., Billinghurst, Z., Depledge, M. H.,2002.4-n-Nonylphenol and17-beta estradiolmay induce common DNA effects in developing barnacle larvae. Environ. Pollut.120,735–738.
[37] Atienzar, F. A., Cordi, B., Donkin, M. E., Evenden, A. J., Jha, A. N., Depledge, M. H.,2000.Comparison of ultraviolet-induced genotoxicity detected by random amplified polymorphic DNAwith chlorophyll fluorescence and growth in a marine macroalgae Palmaria palmata. Aquat. Toxicol.50,1–12.
[38] Becerril, C., Ferrero, M., Sanz, F., Castano, A.,1999a. Detection of mitomycin C-induced geneticdamage in fish cells by use of RAPD. Mutagenesis14(5),449–456.
[39] Bau, D. T., Wang, T. S., Chung, C. H., Wang, A. S., Wang, A. S., Jan, K. Y.,2002. Oxidative DNAadducts and DNA–protein cross-links are the major DNA lesions induced by arsenite. Environ.Health Perspect.110(Suppl.5),753–756.
[40] Becerril, C., Ferrero, M., Sanz, F., Castano, A.,1999b. Detection of mitomycin C-induced geneticdamage in fish cells by use of RAPD. Mutagenesis14,449–456.
[41] Castano, A., Becerril, C.,2004. In vitro assessment of DNA damage after short-and long-termexposure to benzo[a]pyrene usingRAPD and the RTG-2fish cell line. Mutat. Res.552,141–151.
[42] F. A. Atienzar, A. N. Jha, The random amplified polymorphic DNA (RAPD) assay to determine DNAalterations, repair and transgenerational effects in B(a)P exposed Daphnia magna, Mutat. Res.552(2004)125–140.
[43] I. I. Ploskonosiva, V. I. Baranov, A. I. Gaziev, PCR assay of DNA damage and repair at the gene levelin brain and spleen of gamma irradiated young and old rats, Mutat. Res.434(1999)109–117.
[44] C. Quintela-Sabaris, P. S. Kidd, M. I. Fraga, Identification of metal liferous ecotypes of Cistusladanifer L. using RAPD markers, Z. Naturforsch.60(2005)229–235.
[45] C. Conte, I. Mutti, P. Puglisi, DNA fingerprinting analysis by a PCR based method for monitoring thegenotoxic effects of heavy metals pollution, Chemosphere37(1998)2739–2749.
[46] M. R. Enan, Application of randomamplified polymorphicDNA (RAPD) to detect the genotoxiceffect of heavy metals, Biotechnol. Appl. Biochem.43(2006)147–154.
[47] D. H. Blust, T. Backeljau, The population genetic structure of Littorina littorea (Mollusca:Gastropoda) along a pollution gradient in the Scheldt estuary (The Netherlands) using RAPDanalysis, Sci. Total. Environ.325(2004)59–66.
[48] Wan Liua, Y. S. Yangb, c,*, P. J. Li a, Q. X. Zhoua, L. J. Xiea, Y. P. Hana, Risk assessment ofcadmium-contaminated soil on plant DNA damage using RAPD and physiological indices, Journal ofHazardous Materials161(2009)878–883.
[49] Yuan-Cho Lee a, Vivian. C. Yang a, Tsu-Shing Wang b,*, Use of RAPD to detect sodiumarsenite-induced DNA damage in human lymphoblastoid cells, Toxicology239(2007)108–115.
[50]郑永华,蒲富永.汞对鲤鲫鱼组织转氨酶活性的影响[J].西南农业大学学报,1997,19(1):41-45.
[51]贾秀伟,陈志伟.镉对鲫鱼组织转氨酶和过氧化氢酶活性的影响[J].环境污染与防止,1997,19(6):4-7.
[52]陈玉春,顾雪飞,刘敏.5种中草药对鲤血清谷丙转氨酶、谷草转氨酶及红细胞过氧化氢酶活性的影响[J].淡水渔业,2007,37(5):11-13.
[53]陈鹏飞,杨德强,邹红.两种中草药组方对鲫鱼肝脏转氨酶的影响[J].饲料工业,2005,(6):28-31.
[54]张晓红,张虎芳..胭脂红对泥鳅红细胞微核的形成和核异常的影响[J].中国西部科技,2006,3(1):26-28.
[55] Chen Jianjun, Cao Xianglin, Du Qiyan, et al.. Physiological toxicity and genotoxicity of Xingxiangwastewater on loach[J]. Environmental Pollution&Control,2008,30(11):31-34.
[56]张彬彬.乙草胺对泥鳅肝脏谷丙转氨酶和谷草转氨酶的影响[J].江苏农业科学,2009,1:289-290.
[57] LI Yun, RU Shaoguo. Effects of monocrotophos on GPT and GOT activities in the goldfish(Carassius auratus) livers and serum [J]. Journal of Safety and Environment,2008,8(5):9-12.
[58]冯健,刘永坚,田丽霞,等.草鱼实验性镉中毒的肝、肾病理学研究[J].中山大学学报(自然科学版),2003,42(2):226-230.
[59]郑永华,蒲富永.汞对鲤鲫鱼组织转氨酶活性的影响[J].西南农业大学学报,1997,19(1):4l-45.
[60]惠天朝,施明华,朱荫媚.硒对罗非鱼慢性镉中毒肝抗氧化酶及转氨酶的影响[J].中国兽医学报,2000,20(3):264-266.
[61] Chen Jianjun, Cao Xianglin, Du Qiyan, et al.. Physiological toxicity and genotoxicity of Xingxiangwastewater on loach[J]. Environmental Pollution&Control,2008,30(11):31-34.
[62]张彬彬.乙草胺对泥鳅肝脏谷丙转氨酶和谷草转氨酶的影响[J].江苏农业科学,2009,1:289-290.
[63] LI Yun, R. U. Shaoguo. Effects of monocrotophos on GPT and GOT activities in the goldfish(Carassius auratus) livers and serum [J]. Journal of Safety and Environment,2008,8(5):9-12.
[64]王丙莲,张迎梅,侯亚妮,等.镉铅对泥鳅组织转氨酶活性的影响[J].兰州大学学报(自然科学版),2006,4(3):67-70.
[65] Vaglio A., Landriscina C.. Change in liver Enzyme Activity in theTeleost Sparus aurata inResponse to Cadmium Intoxication[J]. Ecotoxicology and Environmental Safety,1999,43:111-116.
[66]徐维娜,谢国驷,刘文斌,等.敌百虫胁迫对异育银鲫鱼体中4种酶活性变化的影响[J].环境科学学报,2008,28(6):1198-1205.
[67]孔力,阎晓红,丁波.金双歧制剂中三种菌苗对大鼠血清GOT、GPT、γ-GT酶活性的影响[J].中国微生态学杂志[J].2000,12(3):183-184.
[68]刘伟,支兵杰,战培荣,等.盐度对大麻哈鱼幼鱼血液生化指标及肝组织的影响[J].应用生态学报,2010,21(9):2411-2417.
[69]刘存歧,刘丽静,王军霞,等.盐碱地渗水钙镁离子对凡纳滨对虾酶活力的影响[J].动物学杂志,2007,42(2):129-133.
[70]王虹扬,黄沈发,徐镜波,等.热污染对金鲫鱼组织内四种酶活性的影响[J].中国环境科学,2006,26(3):372-375.
[71]陈晨,黄峰,舒秋艳,等.共轭亚油酸对草鱼生长、肌肉成分、谷草转氨酶及谷丙转氨酶活性的影响[J].水生生物学报,2010,34(3):647-651.
[72]姚纪花,周平凡.铜、锌和甲胺磷对大鳞副泥鳅胚胎发育和仔鱼成活的影响[J].上海水产大学学报,1997,(1):11-16.
[73] Mckim, J. M.. Evaluation of tests with early life stage of fish for predicting long-term toxicity[J].Fish Ees. Board Can.,1977,34:1148-1154..
[74]贾秀英.镉对泥鳅幼鱼的急性和亚急性毒性研究[J].环境污染与防治,2001,23(5):227-228.
[75] LI Yang, WANG Weimin. Toxicity and Teratogenic Effects of Busulfan in Early DevelopingEmbryo and Larva of Zebrafish (Danio Rerio)[J]. Ecological Science,2008,27(5):368-375.
[76]周立红,陈学豪.四种重金属对泥鳅胚胎和仔鱼毒性的研究[J].厦门水产学院学报,1994,16(1):11-19.
[77]崔可译.汞等六种重金属对鱼卵孵化和仔鱼成活的影响[J].海洋与湖沼,1987,18(2):138-143.
[78] Rice, D. W., Harrison, F. L., and Jearld. A. Jr. Effects of copper of early life history stages ofnorthern anchovy EnCraulis mordax. Fishery Bulletin[J].1980,78(3):675-682.
[79]何斌,何利君,杜军,等.4种重金属离子对淡水石斑胚胎及仔鱼急性毒性的研究[J].水利渔业,2006,24(4):94-95,105.
[80]杨鸢劼.鱼类作为实验动物在环境毒理学研究中的应用[J].水产科技情报,2010,37(4):187-190
[81]陈朝阳,许淼清,谢进金.两种农药对金鱼的急性毒性研究[J].泉州师范学院学报(自然科学),2005,23(6):78-81.
[82]张娜.鱼类急性毒性实验及其条件选择[J].水利渔业,1999,19(6):65-68.
[83]王爱华,苏丹红Ⅰ对小鼠血液和脏器系数的影响,食品科学2010, Vol.31, No.05279,中图分类号: S851.4文献标识码: A文章编号:1002-6630(2010)05-0279-04.
[84] Stiborova M., Frei E., Schmeiger H. H.. Detoxi canon products of the carcinogenic azodye SudanI(Solvent Yellow14) bind to nucleic acids after activation by peroxidase[J]. Cancar Lett,1993,68:43-47.
[85] Stiborova M., Schmeiser H. H., Frei E.. Prostaglandin H synthase medicated oxidation and bindingto DNA of a detoxication metabol i te of carcinogenic Sudan I,1-(phenylazo)-2,6-dihydroxynaphthalene[J]. Cancer Lett,1999,146:53-60.
[86] Stiborovan M., Martinek V., Rydlova H., et al. Expression of cytochrome P4501A1and itscontribution to oxidation of a potential human carcinogen1phenylazo2naphthol(Sudan Ⅰ)inhuman livers[J]. Cancer Letters,2005,220:145-155.
[87]郎朗,于蕾,邹翔.苏丹红I, III, IV致小鼠氧化损伤的实验研究[J].哈尔滨商业大学学报:自然科学版,2005,21(6):687-689.
[88]安玉.苏丹红I号对HepG2细胞的遗传毒性及氧化性DNA损伤[D].大连医科大学,2007.
[89] Holland, N. T. Levine A. J., Smith M. T., et al.. Quantification of epithelial cell micronuclei byfluorescence in situ hybridization (FISH) in mortuary science students exposed to formaldehyde[J].Mutational Research,1996,371:237–248.
[90] Sandra P., Guillamon M., Barcelod D.. Quantitative analysis of polycyclicaromatic hydrocarbons insewage sludge from wastewater treatment plants[J]. Journal of hromatography,2001,938(59):57-65.
[91]郑琰晶,陈琳,陈燕平.十二烷基硫酸钠对水生生物的急性毒性影响[J].农业环境科学学报,2006,25(supl.):496-498.；
[92]杜启艳,吴小华,南平,常重杰。苏丹红Ⅰ对泥鳅红细胞微核率和组织磷酸酶活性的影响[J].安徽农业科学,2008,14:5902-5903
[93] Fischer B, Die experimentelle Erzeugung atypischer Epithelwucherungen unddie Entstehungbosartiger Geschwulste. Med Wochenschr,1906,53:2041
[94]徐厚恩,张铣.卫生毒理学基础[M].北京:北京医科大学中国协和医科大学联合出版社,1991:152-155.
[95]陈怀宇,谢进金,尤晓霞,等.汞对金鱼的急性毒性研究[J].泉州师范学院学报(自然科学),2007,25(6):107-110.
[96]聂晶磊,刘锋,周春玉,等.氯酚类化合物对金鱼的急性和亚急性毒性研究[J].环境科学研究,2001,14(3):6-8.
[97]瞿建国.锌对金鱼的急性毒性及体内的积累和分布[J].上海环境科学,1996,15(6):42—43.
[98]黄周英,谢进金,陈琳钦,等.敌敌畏对金鱼的急性毒性研究[J].毒理学杂志,2005,19(4):311-312.
[99] Guo Fenghong, WANG Zhi-he, CHEN Biwen, et al.. Acute Toxicity of Ammonia and Nitrite toAdult Siniperca chuatsi[J]. Food Science,2009,30(23):397-400.
[100] Hu Xiuzhi, ZHOU Chunjing, WU Ya, et al.. Acute Toxicity Study of Lead and Copper onCarassius auratus[J]. Journal of Neijiang Normal University,2009.24(12):45-48.
[101] Jiang Gangcheng. Study on the Acute Toxicity and Genetics Toxicity of Bensulfuron-methyl onDanio rerio[J]. Journal of Anhui Agricultural Sciences,2009,37(32):15879-15881.
[102] Yang Weidong, SHANG Wen, LIU Jiesheng. Acute Toxicities of Phaeocystis globosa on FiveAquatic Animals[J]. Journal of Tropical and Subtropical Botany,2009,17(1):68-73.
[103]姚纪花,周平凡.铜、锌和甲胺磷对大鳞副泥鳅胚胎发育和仔鱼成活的影响[J].上海水产大学学报,1997,(1):11-16.
[104]李莉,李效宇,孔祥会,等.金鱼胚胎发育的观察研究[J].河南水产,1996,3:24-25.
[105]张毓琪,陈叙龙.环境生物毒理学[M].天津:天津大学出版社,1993,257-258.
[106]惠秀娟.环境毒理学[M].北京:化学工业出版社,2003,270-271.
[107]杜荣骞.生物统计学[M].施普林格出版社,1997.
[108]胡庚东,陈家长,吴伟,等.除草剂丁草胺对黄鳝的遗传毒性[J].湛江海洋大学学报,2005,25(1):43-46.
[109]耿德贵,张大生,程伟,等.四种除草剂对中华大蟾蜍蝌蚪红细胞微核及核异常的影响[J].动物学杂志,2000,35(1):12–16.
[110]周静.离子液体对黑斑蛙胚胎及蝌蚪与隆肛蛙蝌蚪毒性的研究[D].新乡:河南师范大学,2007.
[111]朱毅,张永江.镉、铬、铜及其协同作用对鲤鱼嗜多染红细胞微核的诱发效应[J].南京师大学报(自然科学报),1999,22(3):60-63.
[112] Biggs M. L., Kalman D. A., Moore L. E., et al.. Relationship of urinary arsenium to intakeestimates and a biomarker of effect bladder cell micronucler[J]. Mut Res,1997,386(3):185-195.
[113] Sandra A., Miniss I.. Micronucleus test in erythrocytes of Barbus plebeius(Teleostei Pisces)fromtwo natural envirbarbrments a bioassay for the in situ detection ofmutagens in fresh water[J].Mutation Research/Genetic Toxicology,1996,367(4):245-251.
[114] Mulkiewicz E., JastorffF B., Sk A. C., et al.. Evaluation of the acute toxicity of per fluorinatedcarboxylic acids using eukaryotic cell lines bacteria and enzymatic assays[J]. EnvironmentalToxicology and Phamacologys,2007,23(3):279-285.
[115] Elhajouji A., Cunha M., Kirsch V. M., et al.. Spindle poisons can induce poiyploidy by mitoticslippage and micronucleates in the cytokinesisblock assay[J]. Mutagenesis,1998,13(2):193-198.
[116]汤新慧.除草剂诱发蟾蜍蝌蚪红细胞微核的研究[J].中国环境科学,1998,18(2):162-165.
[117] Lin L, Zeng X L, Zhang J. Effect of profenofos poisoning on liver lipid peroxidation and Liverfunction in rabbits[J]. Clinical Rehabilitation of China,2004,8(21):4380-4381.
[118]王丙莲,张迎梅,侯亚妮,等.镉铅对泥鳅组织转氨酶活性的影响[J].兰州大学学报(自然科学版),2006,4(3):67-70.
[119] Palanivelu V., Vijayavel K., Balasubramanian S. E.. Influence of insecticidal derivative (CartapHydrochloride)from the marinepolychaete on certain enzyme systems of the freshwater fishOreochromis mossambicus[J]. Environ Biol,2005,262:191-195.