胎膜早破孕妇脐血中SOD、MDA、VE、H_2O_2的测定及意义
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摘要
目的:通过对胎膜早破孕妇脐血氧化应激指标—超氧化物歧化酶(SOD)、丙二醛(MDA)、维生素E(VE)及过氧化氢(H2O2)水平的测定,分析氧化应激在胎膜早破发病机制中的作用及意义。
方法: 1研究对象:(1)足月前胎膜早破组:选取2007年10月-2008年6月在河北医科大学第二医院妇产科检查并住院分娩的足月前胎膜早破患者20例,发生在37周以前的称为足月前胎膜早破,胎膜早破诊断标准参照6版《妇产科学》,本组孕妇年龄23-37岁,平均28.38±5.01岁,孕周34+1-36周,平均35±0.75周。(2)足月胎膜早破组:选择同期足月发生胎膜早破者20例,发生在满37周之后的称为足月胎膜早破,本组孕妇年龄26-35岁,平均29.1±3.21岁,孕周38+6-40+3周,平均39.2±0.63周。(3)正常妊娠组:选择同期在我院分娩的正常孕妇20例,年龄25-30岁,平均27.67±1.86岁,孕周38+5-41周,平均39.33±1.21周。所有孕妇均为单胎头位,无妊娠并发症和合并症。
2标本采集:受试对象于胎儿娩出后立即抽取脐静脉血3～5ml,15分钟离心后取血清置-70℃冰箱备用。对每一位受试对象姓名、年龄、体重指数、职业、孕产次、孕周、分娩方式及剖宫产原因,破膜至采集脐血标本的时间等均详细记录,各标本亦标记清楚后存放。
3实验方法:按试剂盒说明操作,MDA采用硫代巴比妥酸(TBA)比色法; SOD活力测定用黄嘌呤、黄嘌呤氧化酶反应系统,以化学发光分析法测定;VE活性采用比色法测定;H2O2采用比色法测定。
4统计学分析:所有数据均采用SPSS13.0进行处理,结果用均数±标准差(—X±s)表示,采用t检验、单因素方差分析,相关分析采用Pearson相关分析,以α=0.05作为显著性检验水准。
结果:
1与正常孕足月妇女相比,40例胎膜早破孕妇脐血氧化指标MDA水平( 15.86±2.33umol/L )和H2O2水平( 126.32±17.58mmol/L )的表达明显高于正常对照组(10.73±4.24 umol/L,109.07±18.93 mmol/L),差异有统计学意义(P < 0.05 , P < 0.05)。而抗氧化指标SOD水平(232.34±20.43 U/ml)和VE水平(4.37±0.85ug/ml)明显低于正常对照组(308.43±22.54 U/ml,6.58±0.39 ug/ml),差异有统计学意义(P<0.05,P<0.05)。
2足月胎膜早破组和足月前胎膜早破组表达水平比较: 20例足月胎膜早破者脐血中的SOD(224.42±20.46 U/ml)、MDA(14.08±2.97 umol/L)、VE(4.67±0.38 ug/ml)和H2O2(119.07±20.37 mmol/L)与20例足月前胎膜早破者脐血中的SOD(230.34±19.23 U/ml)、MDA(13.48±2.09 umol/L)、VE(4.00±0.59ug/ml)和H2O2(120.43±18.08 mmol/L)比较,差异均无统计学意义(P<0.05)。
3在胎膜早破组中,破膜时间对SOD、MDA、VE和H2O2的水平的影响:破膜时间小于12小时的,其SOD水平(251.20±18.42 U/ml)和VE水平(5.43±0.65ug/ml)明显高于破膜时间大于12小时的(221.47±20.62 U/ml,3.55±0.42 ug/ml),差异有统计学意义(P<0.05,P<0.05)。相反,前者的MDA水平( 12.58±1.93umol/L )和H2O2水平(119.37±15.09mmol/L)则明显低于后者(18.59±2.08umol/L, 140.07±17.81mmol/L),差异亦有统计学意义(P<0.05,P<0.05)。
4相关分析结果表明:胎膜早破组和正常妊娠组SOD与MDA(r=-0.512,P<0.01)、H2O2 (r=-0.254,P<0.01)之间呈显著负相关。与VE(r=0.733,P<0.01)呈显著正相关。VE与MDA(r=-0.497,P<0.01)、H2O2 (r=-0.326,P<0.01)呈显著负相关。
结论:1 MDA和H2O2在胎膜早破组的表达水平高于正常妊娠组,表明胎膜早破时氧化应激产物生成增多。SOD和VE在胎膜早破组的表达水平低于正常妊娠组,表明胎膜早破时抗氧化剂的强度相对或绝对的减弱。
2说明胎膜早破患者体内出现了氧化/抗氧化的失平衡,发生了氧化应激。并且氧化应激的强度与发生胎膜早破时的孕周没有关系。
3随着胎膜早破孕妇破膜时间的延长,体内的抗氧化剂水平及活性逐渐下降,而氧化剂水平及活性逐渐增高。说明体内的氧化应激程度与破膜时间有着明显的关系,即随着破膜时间的延长,氧化应激的程度被逐渐放大。
这一发现对于认识胎膜早破发生的病因、预防及治疗均具有重要的意义。
Objective: To determine expression of maternal Cord Blood SOD、MDA、VE and H2O2 in patients with premature rupture of membranes(PROM) in order to analyze their roles and significance in pathogenesis of PROM.
Method: 1 The study subject:(1) The preterm premature rupture of the membrane group: 20 patients with premature rupture of membranes who had prenatal examinations and delivered in the Obstetrics of the Second Hospital of HeBei Medical University were selected from October 2007 to June 2008. Preterm premature rupture of the membranes (P-PROM) is diagnosed when clinically apparent leakage of amniotic fluid is confirmed in pregnant women without uterine contractions or vaginal bleeding before the 37 weeks' gestation..They were diagnosed according to the diagnostic standard (Obstetrics and Gynecology,the Sixth Edition).Mean age of this group was 28.38±5.01 years old (23 to 37 years old),and mean gestational age was 35±0.75 weeks(34+1 to 36 weeks of gestation).(2)The full term premature rupture of the membrane group:20 patients with premature rupture of the membrane after 37w were selected,who were delivered in our hospital in the same time. Mean age of them was 29.1±3.21 years old (26 to 35 years old),and mean gestational age was 39.2±0.63 weeks(38+6 to 40+3 weeks of gestation).(3)normal pregnancy group:20 normal pregnancy march with the two groups were randomly selected. Mean age of them was 27.67±1.86 years old (25 to 30 years old),and mean gestational age was 39.33±1.21 weeks(38+5 to 41 weeks of gestation).All the subjects must meet the following criteria: single pregnancy, head fetal position, with no complications of intered medicine and other complications of pregnancy.
2 Sample collecting: After delivery, draw off 3 ~ 5ml blood in fetal cord blood immediately. 15 minutes centrifugation ,remove serum and reserve them to the refrigerator of -70oC.
Marked every object with its name, age, weight index, occupation, times of pregnancy, gestational weeks, delivery style, reason of cesarean,time from the membrane rupture to collecting the specimen. Every specimen must be signed clearly.
3 The experiment methods: determine the level of index according to the kit specification. The levels of MDA were tested by Thiobarbituric acid reactive substances(TBARS). To assay the levels of SOD by means of xanthine and xanthine oxidase reaction system.The levels of VE and H2O2 were tested by chromatometry.
4 Statistics analysis: All the data were processed by SPSS13.0. All values were expressed as mean±standard (—X±s). Deviation and differences were compared using Student’s t-test and one-way ANOVA. Pearson correlate was made for correlate analysis.α<0.05 was consideredstatistically significant.
Result:
1 Compare with the full-term pregnant woman : the levels of oxidation target MDA ( 15.86±2.33umol/L )and H2O2( 126.32±17.58mmol/L ) in 40 pregnant woman with premature rupture of membranes are higher than the normal control group obviously(10.73±4.24 umol/L,109.07±18.93 mmol/L).. The differences were significant in statistics(P<0.05).But the levels of oxidation resistance target SOD(232.34±20.43 U/ml)and VE (4.37±0.85ug/ml)are lower than the normal control group obviously(308.43±22.54 U/ml,6.58±0.39 ug/ml ) . The differences were significant in statistics(P<0.05).
2 Compare the expression level of the full term premature rupture of membranes with preterm premature rupture of membranes group : For the 20 patients with preterm premature rupture of membranes and 20 patients with full term premature rupture of the membranes, the expression levels of SOD、MDA、VE and H2O2 were no statistical significance(P<0.05).
3 Fetal membrane rupture time effect on the levels of SOD、MDA、VE and H2O2: For the patients whose time less than 12 hours, the SOD leve(l251.20±18.42 U/ml)and VE level(5.43±0.65ug/ml)are higher than the group of the time greater than 12 hours obviously ( 221.47±20.62 U/ml , 3.55±0.42 ug/ml ) .The differences were significant in statistics (P<0.05,P<0.05). On the contrary, the former MDA level(12.58±1.93umol/L)and H2O2 level (119.37±15.09mmol/L)was significantly lower than the latter. The differences were significant in statistics (P<0.05,P<0.05).
4 Correlation analysis results shows: the expression of SOD in normal group and PROM group were negative correlation with MDA(r=-0.512,P<0.01) and H2O2 (r=-0.254,P<0.01) and positive correlation with VE(r=0.733,P<0.01).The expression of VE were negative correlation with MDA(r=-0.497,P<0.01)and H2O2 (r=-0.326,P<0.01).
Conclutions:
1 In PROM group, the expression level of MDA and H2O2 are higher than the normol group, it shows that when premature rupture of membranes there generate a product of increased oxidative stress. The expression level of SOD and VE are lower than the normol group,it shows that when premature rupture of membranes the intensity of antioxidants relatively or absolutely weaken.
2 The patients with premature rupture of membranes in vivo emergence imbalance of oxidant / antioxidant, occurred oxidative stress.
3 Associated with the extension of fetal membrane rupture time, the body's antioxidant levels and activity decreased gradually, and oxidant levels and activity gradually increased.Note that there was a clear relationship with oxidative stress and rupture time.
The discovery have great significance to recognize the causes of premature rupture of membranes, the prevention and treatment .
方法: 1研究对象:(1)足月前胎膜早破组:选取2007年10月-2008年6月在河北医科大学第二医院妇产科检查并住院分娩的足月前胎膜早破患者20例,发生在37周以前的称为足月前胎膜早破,胎膜早破诊断标准参照6版《妇产科学》,本组孕妇年龄23-37岁,平均28.38±5.01岁,孕周34+1-36周,平均35±0.75周。(2)足月胎膜早破组:选择同期足月发生胎膜早破者20例,发生在满37周之后的称为足月胎膜早破,本组孕妇年龄26-35岁,平均29.1±3.21岁,孕周38+6-40+3周,平均39.2±0.63周。(3)正常妊娠组:选择同期在我院分娩的正常孕妇20例,年龄25-30岁,平均27.67±1.86岁,孕周38+5-41周,平均39.33±1.21周。所有孕妇均为单胎头位,无妊娠并发症和合并症。
2标本采集:受试对象于胎儿娩出后立即抽取脐静脉血3～5ml,15分钟离心后取血清置-70℃冰箱备用。对每一位受试对象姓名、年龄、体重指数、职业、孕产次、孕周、分娩方式及剖宫产原因,破膜至采集脐血标本的时间等均详细记录,各标本亦标记清楚后存放。
3实验方法:按试剂盒说明操作,MDA采用硫代巴比妥酸(TBA)比色法; SOD活力测定用黄嘌呤、黄嘌呤氧化酶反应系统,以化学发光分析法测定;VE活性采用比色法测定;H2O2采用比色法测定。
4统计学分析:所有数据均采用SPSS13.0进行处理,结果用均数±标准差(—X±s)表示,采用t检验、单因素方差分析,相关分析采用Pearson相关分析,以α=0.05作为显著性检验水准。
结果:
1与正常孕足月妇女相比,40例胎膜早破孕妇脐血氧化指标MDA水平( 15.86±2.33umol/L )和H2O2水平( 126.32±17.58mmol/L )的表达明显高于正常对照组(10.73±4.24 umol/L,109.07±18.93 mmol/L),差异有统计学意义(P < 0.05 , P < 0.05)。而抗氧化指标SOD水平(232.34±20.43 U/ml)和VE水平(4.37±0.85ug/ml)明显低于正常对照组(308.43±22.54 U/ml,6.58±0.39 ug/ml),差异有统计学意义(P<0.05,P<0.05)。
2足月胎膜早破组和足月前胎膜早破组表达水平比较: 20例足月胎膜早破者脐血中的SOD(224.42±20.46 U/ml)、MDA(14.08±2.97 umol/L)、VE(4.67±0.38 ug/ml)和H2O2(119.07±20.37 mmol/L)与20例足月前胎膜早破者脐血中的SOD(230.34±19.23 U/ml)、MDA(13.48±2.09 umol/L)、VE(4.00±0.59ug/ml)和H2O2(120.43±18.08 mmol/L)比较,差异均无统计学意义(P<0.05)。
3在胎膜早破组中,破膜时间对SOD、MDA、VE和H2O2的水平的影响:破膜时间小于12小时的,其SOD水平(251.20±18.42 U/ml)和VE水平(5.43±0.65ug/ml)明显高于破膜时间大于12小时的(221.47±20.62 U/ml,3.55±0.42 ug/ml),差异有统计学意义(P<0.05,P<0.05)。相反,前者的MDA水平( 12.58±1.93umol/L )和H2O2水平(119.37±15.09mmol/L)则明显低于后者(18.59±2.08umol/L, 140.07±17.81mmol/L),差异亦有统计学意义(P<0.05,P<0.05)。
4相关分析结果表明:胎膜早破组和正常妊娠组SOD与MDA(r=-0.512,P<0.01)、H2O2 (r=-0.254,P<0.01)之间呈显著负相关。与VE(r=0.733,P<0.01)呈显著正相关。VE与MDA(r=-0.497,P<0.01)、H2O2 (r=-0.326,P<0.01)呈显著负相关。
结论:1 MDA和H2O2在胎膜早破组的表达水平高于正常妊娠组,表明胎膜早破时氧化应激产物生成增多。SOD和VE在胎膜早破组的表达水平低于正常妊娠组,表明胎膜早破时抗氧化剂的强度相对或绝对的减弱。
2说明胎膜早破患者体内出现了氧化/抗氧化的失平衡,发生了氧化应激。并且氧化应激的强度与发生胎膜早破时的孕周没有关系。
3随着胎膜早破孕妇破膜时间的延长,体内的抗氧化剂水平及活性逐渐下降,而氧化剂水平及活性逐渐增高。说明体内的氧化应激程度与破膜时间有着明显的关系,即随着破膜时间的延长,氧化应激的程度被逐渐放大。
这一发现对于认识胎膜早破发生的病因、预防及治疗均具有重要的意义。
Objective: To determine expression of maternal Cord Blood SOD、MDA、VE and H2O2 in patients with premature rupture of membranes(PROM) in order to analyze their roles and significance in pathogenesis of PROM.
Method: 1 The study subject:(1) The preterm premature rupture of the membrane group: 20 patients with premature rupture of membranes who had prenatal examinations and delivered in the Obstetrics of the Second Hospital of HeBei Medical University were selected from October 2007 to June 2008. Preterm premature rupture of the membranes (P-PROM) is diagnosed when clinically apparent leakage of amniotic fluid is confirmed in pregnant women without uterine contractions or vaginal bleeding before the 37 weeks' gestation..They were diagnosed according to the diagnostic standard (Obstetrics and Gynecology,the Sixth Edition).Mean age of this group was 28.38±5.01 years old (23 to 37 years old),and mean gestational age was 35±0.75 weeks(34+1 to 36 weeks of gestation).(2)The full term premature rupture of the membrane group:20 patients with premature rupture of the membrane after 37w were selected,who were delivered in our hospital in the same time. Mean age of them was 29.1±3.21 years old (26 to 35 years old),and mean gestational age was 39.2±0.63 weeks(38+6 to 40+3 weeks of gestation).(3)normal pregnancy group:20 normal pregnancy march with the two groups were randomly selected. Mean age of them was 27.67±1.86 years old (25 to 30 years old),and mean gestational age was 39.33±1.21 weeks(38+5 to 41 weeks of gestation).All the subjects must meet the following criteria: single pregnancy, head fetal position, with no complications of intered medicine and other complications of pregnancy.
2 Sample collecting: After delivery, draw off 3 ~ 5ml blood in fetal cord blood immediately. 15 minutes centrifugation ,remove serum and reserve them to the refrigerator of -70oC.
Marked every object with its name, age, weight index, occupation, times of pregnancy, gestational weeks, delivery style, reason of cesarean,time from the membrane rupture to collecting the specimen. Every specimen must be signed clearly.
3 The experiment methods: determine the level of index according to the kit specification. The levels of MDA were tested by Thiobarbituric acid reactive substances(TBARS). To assay the levels of SOD by means of xanthine and xanthine oxidase reaction system.The levels of VE and H2O2 were tested by chromatometry.
4 Statistics analysis: All the data were processed by SPSS13.0. All values were expressed as mean±standard (—X±s). Deviation and differences were compared using Student’s t-test and one-way ANOVA. Pearson correlate was made for correlate analysis.α<0.05 was consideredstatistically significant.
Result:
1 Compare with the full-term pregnant woman : the levels of oxidation target MDA ( 15.86±2.33umol/L )and H2O2( 126.32±17.58mmol/L ) in 40 pregnant woman with premature rupture of membranes are higher than the normal control group obviously(10.73±4.24 umol/L,109.07±18.93 mmol/L).. The differences were significant in statistics(P<0.05).But the levels of oxidation resistance target SOD(232.34±20.43 U/ml)and VE (4.37±0.85ug/ml)are lower than the normal control group obviously(308.43±22.54 U/ml,6.58±0.39 ug/ml ) . The differences were significant in statistics(P<0.05).
2 Compare the expression level of the full term premature rupture of membranes with preterm premature rupture of membranes group : For the 20 patients with preterm premature rupture of membranes and 20 patients with full term premature rupture of the membranes, the expression levels of SOD、MDA、VE and H2O2 were no statistical significance(P<0.05).
3 Fetal membrane rupture time effect on the levels of SOD、MDA、VE and H2O2: For the patients whose time less than 12 hours, the SOD leve(l251.20±18.42 U/ml)and VE level(5.43±0.65ug/ml)are higher than the group of the time greater than 12 hours obviously ( 221.47±20.62 U/ml , 3.55±0.42 ug/ml ) .The differences were significant in statistics (P<0.05,P<0.05). On the contrary, the former MDA level(12.58±1.93umol/L)and H2O2 level (119.37±15.09mmol/L)was significantly lower than the latter. The differences were significant in statistics (P<0.05,P<0.05).
4 Correlation analysis results shows: the expression of SOD in normal group and PROM group were negative correlation with MDA(r=-0.512,P<0.01) and H2O2 (r=-0.254,P<0.01) and positive correlation with VE(r=0.733,P<0.01).The expression of VE were negative correlation with MDA(r=-0.497,P<0.01)and H2O2 (r=-0.326,P<0.01).
Conclutions:
1 In PROM group, the expression level of MDA and H2O2 are higher than the normol group, it shows that when premature rupture of membranes there generate a product of increased oxidative stress. The expression level of SOD and VE are lower than the normol group,it shows that when premature rupture of membranes the intensity of antioxidants relatively or absolutely weaken.
2 The patients with premature rupture of membranes in vivo emergence imbalance of oxidant / antioxidant, occurred oxidative stress.
3 Associated with the extension of fetal membrane rupture time, the body's antioxidant levels and activity decreased gradually, and oxidant levels and activity gradually increased.Note that there was a clear relationship with oxidative stress and rupture time.
The discovery have great significance to recognize the causes of premature rupture of membranes, the prevention and treatment .
引文
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19 Plessinger M A, Woods T R T, Miller R K. Pretreatment of human amnion-chorion with vitamin C and E prevents hypochlorions acid-induced damage[J].AmJ Obstet Gynecol,2000,183(4):979-985
20 Woods Jr JR. Reactive oxygen species and preterm premature rupture of membranes-A review. Placenta 22 supplement A Trophoblast Research 2001;15:S38-44
21 Buonocore G, Perrone S, Longini M, et al. Oxidative stress in preterm neonates at birth and on the seventh day of life. Pediatr Res 2002;52:46-9
22 Wall PD, Pressman EK, Woods Jr JR. Preterm premature rupture of the membranes and antioxidants: the free radical connection. J Perinat Med 2002;30:447-57
23肖文霞,马秀菊.膜早破孕妇血清氧化应激状态分析.国外医学妇幼保健分册。2005,69-70
1 Murr C, Fuith LC, Wridner B, et al. Increased neoptericoncentrations in patients with cancer:indicator of oxidative stress[J]? Anticancer Res,1999,19:1721-1728
2 Niwa T, Naito C, Hassan A, et al. Increased glutathionyl hemoglobin in diabetes mellitus and hyperlipidemia demon-strated by liquid chromatography/electrospray lonizationmass spectrometry[J]. Clin Chem,2000,46:82-88
3 Paolisso G, Eeposito R, D’Alessio MA, et al.Primary andsecondary prevention of atherosclesis:is there a role for antioxidants[J]? Diabetes Metab,1999,25:298-306
4 Muzykantov VR.Tavgeting of superoxide dismutase and catalase to vascular endothelilm,Control Release,2001, 71:6-21
5 Jenkins C, Wilson R, Roberts J,et al. Antioxidants: their role in pregnancy and miscarriage[J]. Antioxid Redox Signal,2000,2(3):623-628
6 Qanungo S, Mukherjea M. Ontogenic profile of some antioxidants and lipid peroxidation in human placental and fetal tissues[J]. Mol Cell Biochem,2000,215(1-2):11-19
7 Azzi A, Boscoboinik D, Hensey C. The protein kinase C family [J].Eur J Biochem, 1992, 208(3): 547-557
8 Bursell SE, George L, King. The potential use of glutathionyl hemoglobin as a clinical marker of oxidative stress[J]. Clin Chem,2000,46:145-146
9唐爱华·巨内皮素-1的研究进展·国外医学临床生物学与检验学分册[J],1998,19(4):147-148
10 Pennathur S, Jackson-lewis V, Przedborski S, et al. Mass spectrometric quantification of 3-nitrotyosine,o-tyrosine,and o,o’-dityrosine in brain tissue of 1-methy l-4-pheny -1,2,3, 6-tetrahydropyridine-treated mice, a model of oxidative stress in Parkinson’s disease[J]. J Biol Chem 1999, 274: 34621-34628
11王文杰等.生理科学进展,1985,16(3):196-198
12 Buege JA, Aust SD. Microsomal lipid perioxidation. Methods Enzymol, 1978, 30: 302-308
13 Messent M, Griffiths M J, Quinlan G J,et a.l Ischaemia-reperfusion injury in the rat ismodulated by superoxide generation and leads to an augmentation of the hypoxic pulmonary vascular response[J].Clin Sci (Lond), 1996, 9(1): 47-54
14 Konishi A, Aizawa T, Mohan A, et a.l Hydrogen peroxide activates the Gas6-Axl pathway in vascular smooth muscle cells[ J]. J Biol Chem, 2004, 27 (27): 28766-20770
15 Li J, Li W, Su J, et a.l Hydrogen per-oxide induces apoptosis in cerebral vascular smooth muscle cells: possible relation to neurodegenerative diseases and strokes[ J]. Brain Res Bul,l 2003, 62(2): 101-106
16 Wall PD, Pressman EK, Woods JR Jr-Preterm premature rupture of the membranes and antioxidants: the free radical connection[J]. J Perinat Med,2002,30(6):447-457
17 Plessinger MA, Woods JJ, Miller RK. Pretreatment of human amnion-chorion with vitamin C and E prevents hypochlorions acid-induced damage [J]. Am J Obstet Gynecol,2000,183(4):979-985
18 Hampson V,Liu D,Billett E,et al.Br J Obstet Gyanecol, 1997,104(9):1081-1091
19 Artal R,Burgeson R,Fernandez FG,et al.Copper levels and premature rupture of membrane.Obstel Gynecol, 1979, 53:608
20 Woods Jr JR. Reactive oxygen species and preterm premature rupture of membranes-A review. Placenta 22 supplement A Trophoblast Research 2001;15:S38-44
21 Buonocore G, Perrone S, Longini M, et al. Oxidative stress in preterm neonates at birth and on the seventh day of life. Pediatr Res 2002;52:46-9
22 Wall PD, Pressman EK, Woods Jr JR. Preterm premature rupture of the membranes and antioxidants: the free radical connection. J Perinat Med 2002;30:447-57
23肖文霞,马秀菊.膜早破孕妇血清氧化应激状态分析.国外医学妇幼保健分册。2005,69-70
2 Beck MA. Selenium and host defence towards viruses. Proc Nutr Soc,1999, 58(3): 707-711
3 zaki M, Deshpande SS, AngkeowP, et al. Inhibitionof the Rac1 GT-Pase protects against nonlethal ischrmia/ reperfusion-induced necrosis and apoptosis in vivo. FASEBJ, 2000, 14: 418-429
4 Azzi A, Boscoboinik D, Hensey C. The protein kinase C family [J].Eur J Biochem, 1992, 208(3): 547-557
5 Buege JA, Aust SD. Microsomal lipid perioxidation. Methods Enzymol, 1978, 30: 302-308
6 Messent M, Griffiths M J, Quinlan G J,et a.l Ischaemia-reperfusion injury in the rat ismodulated by superoxide generation and leads to an augmentation of the hypoxic pulmonary vascular response[J].Clin Sci (Lond), 1996, 9(1): 47-54
7 Konishi A, Aizawa T, Mohan A, et a.l Hydrogen peroxide activates the Gas6-Axl pathway in vascular smooth muscle cells[ J]. J Biol Chem, 2004, 27 (27): 28766-20770
8 Li J, Li W, Su J, et a.l Hydrogen per-oxide induces apoptosis in cerebral vascular smooth muscle cells: possible relation to neurodegenerative diseases and strokes[ J]. Brain Res Bul,l 2003, 62(2): 101-106
9 Myatt L,Cuix.Oxidative stress in the placenta[J]. HistocheCell Biol,2004,122(4):369-382
10 Burlingame J M,Esfandiari N,Sharma R K,et al.Tota antioxidant capacity and reactive oxygen species in amniotic fluid[J].Obstet Gynecol,2003,101(4):756-761
11 Wisdom SJ,Wilson R,Mckillop JH,et al.Antioxidant systems innormal pregnancy and in pregnancy-induced hypertension. Am J Obstet Gynecol,1991,165:1701
12 Hiromichi Shoji,and Berthold Koletzko. Oxidative stressand antioxidant protection in the perinatal period. Current Opinion in Clinical Nutrition and Metabolic Care 2007, 10:324-328
13唐敏一编著.胎盘病理学[M].第1版.北京:人民卫生出版社,1987,48-68
14 Stuart EL, Evans GS, Lin YS,et al. Reduced collagen and ascorbic acid concentrations and increased proteolytic susceptibility with prelabor foetal membrane rupture in women. Biol Reprod 2005;72:230-5
15 Macdermott RI, Landon CR. The hydroxyproline content of amnion and prelabour rupture of the membranes. Eur J Obstet Gynecol Reprod Biol 2000;92:217-21
16赖仁胜,周溶,李祥周,等.胎膜早破的生物物理学机理探讨.中华妇产科杂志,1993,28:520
17 Hampson V,Liu D,Billett E,et al.Br J Obstet Gyanecol,1997,104(9):1081-1091
18 Artal R,Burgeson R,Fernandez FG,et al.Copper levels and premature rupture of membrane.Obstel Gynecol, 1979, 53:608
19 Plessinger M A, Woods T R T, Miller R K. Pretreatment of human amnion-chorion with vitamin C and E prevents hypochlorions acid-induced damage[J].AmJ Obstet Gynecol,2000,183(4):979-985
20 Woods Jr JR. Reactive oxygen species and preterm premature rupture of membranes-A review. Placenta 22 supplement A Trophoblast Research 2001;15:S38-44
21 Buonocore G, Perrone S, Longini M, et al. Oxidative stress in preterm neonates at birth and on the seventh day of life. Pediatr Res 2002;52:46-9
22 Wall PD, Pressman EK, Woods Jr JR. Preterm premature rupture of the membranes and antioxidants: the free radical connection. J Perinat Med 2002;30:447-57
23肖文霞,马秀菊.膜早破孕妇血清氧化应激状态分析.国外医学妇幼保健分册。2005,69-70
1 Murr C, Fuith LC, Wridner B, et al. Increased neoptericoncentrations in patients with cancer:indicator of oxidative stress[J]? Anticancer Res,1999,19:1721-1728
2 Niwa T, Naito C, Hassan A, et al. Increased glutathionyl hemoglobin in diabetes mellitus and hyperlipidemia demon-strated by liquid chromatography/electrospray lonizationmass spectrometry[J]. Clin Chem,2000,46:82-88
3 Paolisso G, Eeposito R, D’Alessio MA, et al.Primary andsecondary prevention of atherosclesis:is there a role for antioxidants[J]? Diabetes Metab,1999,25:298-306
4 Muzykantov VR.Tavgeting of superoxide dismutase and catalase to vascular endothelilm,Control Release,2001, 71:6-21
5 Jenkins C, Wilson R, Roberts J,et al. Antioxidants: their role in pregnancy and miscarriage[J]. Antioxid Redox Signal,2000,2(3):623-628
6 Qanungo S, Mukherjea M. Ontogenic profile of some antioxidants and lipid peroxidation in human placental and fetal tissues[J]. Mol Cell Biochem,2000,215(1-2):11-19
7 Azzi A, Boscoboinik D, Hensey C. The protein kinase C family [J].Eur J Biochem, 1992, 208(3): 547-557
8 Bursell SE, George L, King. The potential use of glutathionyl hemoglobin as a clinical marker of oxidative stress[J]. Clin Chem,2000,46:145-146
9唐爱华·巨内皮素-1的研究进展·国外医学临床生物学与检验学分册[J],1998,19(4):147-148
10 Pennathur S, Jackson-lewis V, Przedborski S, et al. Mass spectrometric quantification of 3-nitrotyosine,o-tyrosine,and o,o’-dityrosine in brain tissue of 1-methy l-4-pheny -1,2,3, 6-tetrahydropyridine-treated mice, a model of oxidative stress in Parkinson’s disease[J]. J Biol Chem 1999, 274: 34621-34628
11王文杰等.生理科学进展,1985,16(3):196-198
12 Buege JA, Aust SD. Microsomal lipid perioxidation. Methods Enzymol, 1978, 30: 302-308
13 Messent M, Griffiths M J, Quinlan G J,et a.l Ischaemia-reperfusion injury in the rat ismodulated by superoxide generation and leads to an augmentation of the hypoxic pulmonary vascular response[J].Clin Sci (Lond), 1996, 9(1): 47-54
14 Konishi A, Aizawa T, Mohan A, et a.l Hydrogen peroxide activates the Gas6-Axl pathway in vascular smooth muscle cells[ J]. J Biol Chem, 2004, 27 (27): 28766-20770
15 Li J, Li W, Su J, et a.l Hydrogen per-oxide induces apoptosis in cerebral vascular smooth muscle cells: possible relation to neurodegenerative diseases and strokes[ J]. Brain Res Bul,l 2003, 62(2): 101-106
16 Wall PD, Pressman EK, Woods JR Jr-Preterm premature rupture of the membranes and antioxidants: the free radical connection[J]. J Perinat Med,2002,30(6):447-457
17 Plessinger MA, Woods JJ, Miller RK. Pretreatment of human amnion-chorion with vitamin C and E prevents hypochlorions acid-induced damage [J]. Am J Obstet Gynecol,2000,183(4):979-985
18 Hampson V,Liu D,Billett E,et al.Br J Obstet Gyanecol, 1997,104(9):1081-1091
19 Artal R,Burgeson R,Fernandez FG,et al.Copper levels and premature rupture of membrane.Obstel Gynecol, 1979, 53:608
20 Woods Jr JR. Reactive oxygen species and preterm premature rupture of membranes-A review. Placenta 22 supplement A Trophoblast Research 2001;15:S38-44
21 Buonocore G, Perrone S, Longini M, et al. Oxidative stress in preterm neonates at birth and on the seventh day of life. Pediatr Res 2002;52:46-9
22 Wall PD, Pressman EK, Woods Jr JR. Preterm premature rupture of the membranes and antioxidants: the free radical connection. J Perinat Med 2002;30:447-57
23肖文霞,马秀菊.膜早破孕妇血清氧化应激状态分析.国外医学妇幼保健分册。2005,69-70