Antioxidant systems in rat lens as a function of age: effect of chronic administration of vitamin E and ascorbate.

Oxidative damage occurring in the lenses of patients with senile cataract may be due to partially reduced forms of oxygen. We assayed the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Red), and glucose-6-phosphate dehydrogenase (G6PD) in rat lenses at different ages (1, 4, and 24 months), and also evaluated lens glutathione (GSH) levels and the effects of chronic administration of vitamin E and sodium ascorbate. We observed a significant age-related decrease in GSH-Px, GSH-Red and G6PD activities, but no age-related change in SOD activity. Chronic treatment with both vitamin E and sodium ascorbate failed to restore enzymatic activities to the levels of younger rats. An age-related reduction in GSH content was also observed; however, chronic administration of vitamin E, but not of sodium ascorbate, restored GSH levels to those of younger rats.     

维生素E对小鼠慢性乙醇性肝损害的保护作用

目的 探讨乙醇性肝损害的发病机制，并研究维生素E对乙醇性肝损害的保护作用。方法 昆明种小鼠30只，分为三组：正常对照组（自由饮水，不做其他处理）、乙醇组（自由饮用2．5％乙醇8周）、乙醇＋维生素E组（自由饮用2．5％乙醇8周，同时经口给予维生素E200mg/kg，每天1次，共8周）。分别测定血清丙氨酸转氨酶、肝匀浆蛋白含量、肝匀浆丙二酰乙醛含量及肝匀浆超氧化物歧化酶、过氧化氢酶、谷胱甘肽、谷胱甘肽－S－转移酶、谷胱甘肽还原酶、谷胱甘肽过氧化酶的活性。结果 摄入乙醇8周后多种抗氧化酶及抗氧化物发生改变，维生素E可拮抗乙醇的上述作用，使指标的改变发生逆转。结论 维生素E对慢性乙醇性肝损害的保护作用。     

Moderate exercise with a dietary vitamin C and e combination protects against streptozotocin-induced oxidative damage to the kidney and lens in pregnant rats.

Moderate exercise and vitamin C and E (VCE) supplementation can be beneficial to diabetes due to reducing free radical production in lens and kidney of diabetic pregnant rats. We investigated the effect of VCE supplementation and moderate exercise on lipid peroxidation (MDA) and scavenging enzyme activity in the kidneys and lens of STZ-induced diabetic pregnant rats. Fifty female Wistar rats were used and were randomly divided into five groups. First and second were used as the control and pregnant control group. Third group was the pregnant diabetic group. The fourth group was the diabetic-pregnant-exercise group. VCE-supplemented feed was given to pregnant-diabetic-exercise rats constituting the fifth group. Animals in the exercised groups were moderately exercised daily on a treadmill (16.1 m/min, 45 min/d) for three weeks (five days a week). Diabetes was induced on day zero of the study. Plasma, lens, and kidney samples were taken from all animals on day 20. Exercise and administration of VCE to pregnant diabetic rats resulted in significant decrease in the albumin and total protein values and the elevated MDA, plasma creatinine, and urea levels as an indicator of oxidative stress and renal functional parameters. Exercise and VCE supplementation also increased glutathione peroxidase (GSH-Px), reduced glutathione (GSH), vitamin E, and beta-carotene levels in the kidney, GSH-Px and GSH in the lens, the albumin and total protein values in plasma. In the diabetic pregnant animals, the decreased vitamins A and E concentration and GSH levels in kidney, creatinine, and urea values in plasma did not improve through exercise only although their concentrations were increased by VCE supplementation. Kidney weight did not also affect either by exercise or VCE supplementation. In conclusion, these results suggest that exercise plus VCE affects antioxidant metabolism and reduces lipid peroxidation, thereby improving the damage caused by oxidative stress involved in the pathogenesis of lens and kidney in diabetic pregnant rats. Moderate exercise with dietary VCE may play a role in preventing nephropathy and cataract formation in diabetic pregnant rat.     

维生素E修饰透析膜对血液透析患者红细胞抗氧化应激的效果

目的　观察VitE修饰的透析膜 (CL E)对血透患者红细胞生成素 (rH EPO)疗效的影响。方法　选 40名血透患者停EPO一个月 ,并随机分为二组 ,A组 ( 2 0例 )用CL E ;B组 ( 2 0例 )用常规透析膜 ,观察 6周。实验开始时两组同时给与同样剂量 (每周 15 0IU/kg)rH EPO治疗 ,分别于实验第 1、4、7、10、13、16、19次透析前测血常规 ,第 7、19次透析前取空腹血 ,测定血浆和红细胞中丙二醛 (MDA)、VitE及红细胞中谷胱甘肽 (GSH)、过氧化物歧化酶 (SOD)浓度。结果　实验结束时A组血浆VitE水平比实验前明显升高 ,MDA明显下降 ;红细胞中VitE、GSH及SOD明显升高 ,MDA明显下降 (P均 <0 .0 5 )。B组实验前后无明显变化。A组Hb水平在实验 4周时较实验前明显提高(P <0 .0 5 ) ,B组在 6周时发现 ,A组Hct水平在实验 3周时较实验前明显提高 (P <0 .0 5 ) ,B组在 5周时才出现。结论　CL E有抗氧化作用 ,使rH EPO的升血作用提前出现 ,促进其升血效果     

The effect of carnosine treatment on prooxidant–antioxidant balance in liver,heart and brain tissues of male aged rats

Carnosine (β-alanyl-l-histidine) is a dipeptide with antioxidant properties. Oxidative damage by free radicals is one of the mechanisms underlying the aging process. This study was done to investigate the effects of carnosine treatment on lipid peroxidation and antioxidant status of liver, heart, brain in male young and aged rats. At the initiation of study, young and aged rats were 5 and 22 months old, respectively. Carnosine (250 mg/kg, daily, i.p.) was administered for 1 month to rats. At the end of this period, malondialdehyde (MDA) and diene conjugate (DC) and protein carbonyl (PC) levels, glutathione (GSH), vitamin E and vitamin C levels and Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities were determined in tissues of carnosine-treated young and old rats. Liver and heart, but not brain MDA and DC levels increased significantly in aged rats as compared to young rats. Liver PC levels were also significantly elevated. Significant decreases in GSH and vitamin C levels and SOD activities were detected in liver of aged rats, but vitamin E levels and GSH-Px and GST activities remained unchanged. Non-enzymatic and enzymatic antioxidants did not change in heart and brain of aged rats. Carnosine treatment decreased high MDA, DC and PC levels and caused significant increases in vitamin E level and SOD activity in the liver of aged rats. There were no changes in non-enzymatic and enzymatic antioxidants in the heart and brain of carnosine-treated aged rats. In conclusion, carnosine treatment was found to be useful in the decrease of age-related oxidative stress in the liver.     

年龄相关性白内障晶状体上皮细胞中miR-181a和SIRT1的表达关系及意义

目的探讨白内障晶状体上皮细胞微小RNA-181a(miR-181a)与沉默信息调节因子(SIRT)1的表达关系,研究其在年龄相关性白内障患者的诊治及病情评估方面的临床意义。方法选取诊断为年龄相关性白内障患者62例为白内障组,另选取同期近视矫正手术患者42例为对照组,利用RT q-PCR法,检测两组晶状体上皮细胞miR-181a与SIRT1表达水平;Pearson法测定miR-181a与SIRT1相关性;利用Lipofectamine 2000转染miR-181a模拟物和抑制剂,调节人晶状体上皮细胞miR-181a表达水平,RT q-PCR法检测SIRT1表达水平;酶联免疫吸附试验(ELISA)检测晶状体上皮细胞中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱氨酸(GSH)、谷胱氨酸过氧化物酶(GSH-Px)水平。结果与对照组相比,白内障组miR-181a表达水平显著升高,SIRT1表达水平显著降低(P<0.05);Pearson相关分析显示,miR-181a和SIRT1呈负相关关系(r=-0.719,P<0.05);miR-181a模拟物组SIRT1表达水平显著低于模拟物阳性对照组(P<0.05),miR-181a抑制剂组,SIRT1表达水平显著高于抑制剂阴性对照组(P<0.05);白内障组SOD、GSH、GSH-Px水平明显低于正常组(P<0.05),MDA水平明显高于正常组(P<0.05);miR-181a表达水平与SOD、GSH、GSH-Px因子呈负相关关系(r=-0.702,-0.739,-0.776),与MDA水平呈正相关关系(r=0.679);SIRT1表达水平与SOD、GSH、GSH-Px呈正相关关系(r=0.699,0.743,0.763),与MDA水平呈负相关关系(r=-0.684)。结论白内障晶状体上皮细胞中miR-181a高表达,SIRT1低表达,miR-181a可调控人晶状体上皮细胞中SIRT1表达;SIRT1低表达可促使晶状体上皮细胞凋亡,从而影响或导致了年龄相关性白内障的发病。     

维生素E修饰的透析膜抗氧化作用临床研究

目的　观察维生素E(VitE)修饰的透析膜 (Cl E)的抗氧化作用。方法　选择 2 0 0 3- 0 5～ 2 0 0 3- 0 7首都医科大学附属友谊医院住院的 5 7名血透患者随机分为 3组。A组Cl E ;B组常规透析膜同时服VitE(每天4 0 0mg) ;C组常规透析膜 ,观察 4周。第 1、13次透析前抽血 ,测血浆和红细胞中丙二醛 (MDA )、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶 (GSH px)、过氧化物歧酶 (SOD)、VitE及血浆晚期氧化蛋白质终末产物 (AOPP)。结果　A组观察结束后血浆和红细胞中VitE、GSH px、GSH及SOD比观察前升高 ,MDA及AOPP(红细胞中未测 )下降 ,差异有显著性 (P <0 0 5 )。B组红细胞中VitE比观察前升高 ,血浆和红细胞中MDA下降 ,差异有显著性 (P <0 0 5 ) ,其余指标无明显变化。C组实验前后各指标无明显变化 (P >0 0 5 )。结论　透析患者使用VitE有抗氧化作用 ,用Cl E透析比口服VitE效果更好。     

Impairment of Intestinal Mucosal Antioxidant Defense System During Salmonella typhimurium Infection

The mucosal pathology of Salmonella typhimuriuminfection may in part be due to the excessive productionof reactive oxygen species (ROS). The influence of S.typhimurium infection on the intestinal mucosal antioxidant defense system was investigated. Weinjected ligated rat ileal loops with Salmonella liveculture or toxin. After 18 hr of infection, the animalswere killed and enterocytes isolated from the ileal loops. The enterocyte-reduced glutathione(GSH) content and activities of the enzymes superoxidedismutase (SOD), glutathione peroxidase (GSH-Px),catalase, glutathione-S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphatedehydrogenase (G6PDH) were spectrophotometricallyestimated. The vitamin E and A contents were determinedby high-performance liquid chromatography (HPLC). Inboth the Salmonella live culture and toxin-treatedgroups, the enterocyte GSH and vitamin E contents andactivities of the enzymes SOD, GSH-Px, catalase, GR, andG6PDH were significantly decreased as compared to the control group. However there was asignificant increase in the enterocyte activity of GST.There was no change in the vitamin A content of theenterocytes. These findings might indicate a decreased endogenous intestinal protection against ROS inS. typhimurium-mediated infection, which couldcontribute to the pathogenesis of the disease.     

曲美他嗪对大鼠缺血再灌注心肌线粒体的保护作用

目的探讨曲美他嗪对缺血再灌注损伤心肌线粒体的保护作用及其机制.方法将50只SD雄性大鼠随机分为假手术组、生理盐水组和曲美他嗪组(5mg/kg组及10mg/kg组)4组,假手术组只开胸,不结扎冠状动脉.余3组复制缺血再灌注损伤模型,缺血前分别静脉注射曲美他嗪(5或10mg/kg)及等量生理盐水,在缺血30min及再灌注40min时测定缺血再灌注损伤区心肌线粒体丙二醛、超氧化物歧化酶、谷胱甘肽、谷胱甘肽过氧化物酶及总钙浓度,并通过电镜观察心肌超微结构的改变.结果与假手术组比较,生理盐水组及曲美他嗪组线粒体中的丙二醛及总钙显著增高,超氧化物歧化酶、谷胱甘肽及谷胱甘肽过氧化物酶显著降低.与生理盐水组比较,曲美他嗪组的丙二醛及总钙水平显著降低,超氧化物歧化酶、谷胱甘肽及谷胱甘肽过氧化物酶显著增高.电镜观察显示曲美他嗪组线粒体损伤较生理盐水组明显减轻.结论以上提示曲美他嗪能减轻缺血再灌注心肌线粒体的脂质过氧化损伤,其机制可能是通过提高线粒体内谷胱甘肽含量及超氧化物歧化酶和谷胱甘肽过氧化物醇活性,以增强其抗氧化能力,并通过减轻线粒体内钙聚积在细胞水平提供心肌保护作用.     

The correlation between markers of oxidative stress and risk factors of coronary artery disease in Thai patients

An imbalance between oxidative damage and antioxidative protection in association with the pathophysiology of atherosclerosis has been suggested. The aim of our study was to investigate the relationship between plasma lipids, the antioxidant system and oxidative damage in Thai patients with stable coronary artery disease (CAD). Sixty-one patients (40 males, 21 females), who were angiographically defined as having CAD and were clinically stable, participated in this study. Thirty-two healthy subjects (20 males, 12 females) served as normal controls. The investigation included the measurements of plasma lipid profiles and plasma total antioxidative status (TAS) such as plasma vitamin E erythrocyte glutathione (GSH) and glutathione peroxidase (GPx), as well as malondialdehyde (MDA) and total plasma total protein thiols (P-SH). In patients with CAD, erythrocyte GSH and GPx were significantly lower than those found in controls. However plasma TAS and vitamin E were not significantly different between groups. Patients with CAD also had higher MDA and lower P-SH levels than the controls, which represents the oxidative damage products of lipid and proteins. Multiple regression analysis revealed negative correlations between GSH and cholesterol, GSH and low density lipoprotein (LDL), vitamin E and MDA, as well as P-SH and MDA. This study demonstrated the status of oxidative stress in patients with stable CAD. Since oxidative stress is the imbalance between the total oxidants and antioxidants in the body, any single oxidant/antioxidant parameter may not reflect the overall oxidative stress system. Thus, in patients with CAD, diets with various types of antioxidants may be more beneficial in increasing antioxidant activity than any particular antioxidant supplementation.     

Milk whey protein decreases oxygen free radical production in a murine model of chronic iron-overload cardiomyopathy

BACKGROUND: Chronic iron overload is a major cause of organ failure worldwide, but its pathogenesis remains to be elucidated. OBJECTIVES: To examine in an experimental murine model of iron-overload cardiomyopathy the relation between milk whey protein and, first, the production of reactive oxygen free radical species and, second, antioxidant reserve status. METHODS: B6D2F1 mice were randomly assigned to four treatment groups (n=8 per treatment group): placebo control; iron only; whey only; and iron with whey. Reactive oxygen free radical species in the heart were quantified by the cytotoxic aldehydes malondialdehyde (MDA), 4-hydroxy-nonenal (HNE) and hexanal, while antioxidant reserve status was quantified by glutathione (GSH) and glutathione peroxidase (GPx) activity in the heart tissue. RESULTS: Significantly decreased concentrations (pmol/100 mg wet weight tissue) of MDA (2468+/-261), HNE (912+/-38) and hexanal (5385+/-927) were observed in the heart tissue of the group receiving iron with whey, in comparison with the iron-only treatment group (MDA 9307+/-387, HNE 1416+/-157, hexanal 14,874+/-2955; P<0.001). Significantly increased GPx (141+/-38 IU/L) and GSH (521+/-136 IU/L) activity were observed in mice receiving iron with whey, in comparison with mice receiving iron only (GPx 100+/-10 IU/L, GSH 446+/-33 IU/L; P<0.001). CONCLUSION: Mice receiving iron treatments with whey supplementation had significantly lower concentrations of cytotoxic aldehydes and significantly higher cardiac levels of GPx and GSH activity than did iron-only treated mice. Additional basic research is warranted to examine the exact mechanisms by which milk whey protein protects the heart.     

绞股蓝总皂苷对四氯化碳诱导大鼠肝纤维化的防治作用

目的:观察绞股蓝总皂苷对四氯化碳( CCl4)诱导的大鼠肝纤维化的防治作用.方法:采用CCl4诱导的大鼠肝纤维化模型,分为正常组(Z,n=6)、模型组(M,n=8)、绞股蓝总皂苷组(J,n=8)、秋水仙碱(Q,n=8).造模6周末开始给药(股蓝总皂苷200mg/kg体重、秋水仙碱0.1mg/kg体重),给药3周.观察:①大鼠体重、肝脾比值的变化;②血清丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、谷氨酰转肽酶(GGT)活性、白蛋白( Alb)、总胆红素(TBil)含量、肝组织羟脯氨酸(Hyp)含量;③肝组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)、还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)含量;④肝组织病理及胶原沉积情况.结果:①M组大鼠血清ALT、AST、GGT、TBil显著升高,Alb显著降低;J和Q组大鼠血清ALT、AST、GGT、TBil显著下降,Alb显著升高;②M组大鼠肝组织Hyp含量显著升高,J组及Q组大鼠肝组织Hyp含量显著下降;③肝组织HE染色显示:M组大鼠肝细胞脂肪变性,大量纤维结缔组织增生,假小叶形成.J组及Q组大鼠肝细胞脂肪变性减轻,纤维增生减少,少见完整假小叶结构.天狼星红染色显示:M组大鼠肝窦周胶原沉积明显,形成较厚汇管区和中央静脉间的纤维间隔,J组和Q组大鼠肝脏汇管区胶原纤维染较M组明显减轻;④M组大鼠肝组织SOD活性及GSH含量明显降低,MDA含量显著升高.J组大鼠肝组织SOD活性显著提高.结论:绞股蓝总皂苷具有显著抗CCl4诱导的大鼠肝纤维化及氧化损伤的作用.     

褪黑素对糖尿病患者氧化应激抑制作用和糖脂代谢影响的观察

目的 探讨褪黑素对糖尿病患者氧化应激的抑制作用及糖脂代谢的影响。 方法 1998-12～2003-04东南大学附属中大医院采用随机、单盲、安慰剂平行对照的方法,观察褪黑素及安慰剂对91例糖尿病患者血清丙二醛(MDA)及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的影响,并分析上述影响与糖脂代谢变化之间的关系。 结果 治疗前糖尿病患者血清SOD、GSH-Px水平下降,MDA水平上升。褪黑素组8周处理后血清SOD和GSH-Px水平上升,而MDA水平明显下降,与处理前相比差异有显著;安慰剂组处理前后患者血清SOD、GSH-Px及MDA水平无明显变化。褪     

Increased plasma levels of glutathione and malondialdehyde after acute ethanol ingestion in humans

The effect of acute ethanol consumption on plasma glutathione (GSH) and malondialdehyde (MDA) concentrations was studied in two groups of healthy male subjects. The first group (n = 15) received an acute dose of ethanol (1.5 g/kg p.o. over a period of 3 h); in the control group (n = 15), ethanol was replaced isocalorically with carbohydrates. Blood samples were taken at 0 time (ethanol/carbohydrates ingestion) and every 60 min for 6 h. A significant increase in plasma MDA concentration as well as in plasma GSH values were observed in subjects receiving ethanol compared to controls. The enhancement of plasma GSH was accompanied by a concomitant increase of oxidized glutathione (GSSG). These data support the hypothesis of an increase of lipid peroxidation as a possible mechanism of acute ethanol toxicity. The enhancement of plasma GSH and GSSG may reflect an increased utilization and loss of the tripeptide from the liver induced by ethanol.     

The effects of antioxidants on exercise-induced lipid peroxidation in patients with COPD

OBJEctive: The oxidant-antioxidant balance plays an important role in the pathogenesis of COPD. The aim of the present study was to evaluate the effects of exercise, as an oxidative stress factor on the oxidant-antioxidant balance and to investigate whether short-term antioxidant treatment affects lipid peroxidation products. METHODOLOGY: Twenty-one stable COPD patients and 10 control subjects were included in the study. Symptom-limited exercise tests were performed by all subjects. Blood was collected before and 1 h after exercise in control subjects and before, 1 and 3 h after exercise in COPD patients, for analysis of malondialdehyde (MDA), reduced glutathione (GSH) and vitamin E (VE) levels. VE and vitamin C treatments were added to the regular bronchodilator therapy in 10 COPD patients for 1 month. After the treatment period, an exercise test was performed and blood was collected again for MDA, GSH and VE levels. RESULTS: Baseline GSH and VE levels were significantly lower in the COPD group when compared with the control subjects. There was no statistically significant difference in MDA levels between the two groups. In the COPD group, MDA levels 3 h after exercise were significantly higher than at baseline. In contrast there were no significant differences in MDA, VE and GSH levels in the control group after exercise. VE and MDA levels increased significantly after exercise in COPD patients but there was no difference in GSH levels. Baseline exercise time was significantly lower in the COPD group than in the controls. In 10 COPD patients who were given antioxidant therapy, their exercise time increased significantly and there was no increase in MDA and VE levels after the repeated exercise test. CONCLUSIONS: Antioxidant levels were significantly lower in COPD patients than in control subjects. In these patients, exercise results in more significant oxidative stress and lipid peroxidation than in control subjects and antioxidant therapy may decrease lipid peroxidation following exercise and improve exercise capacity.     

还原型谷胱甘肽对正加速度暴露下急性胃黏膜损伤大鼠胃黏膜的影响

目的研究还原型谷胱甘肽(GSH)对正加速度(+Gz)暴露下急性胃黏膜损伤大鼠胃黏膜的影响及可能机制。方法 40只雄性SD大鼠随机分成4组:无水乙醇对照组(A组)、+5 Gz值暴露组(B组)、+10 Gz值暴露组(C组)、GSH预处理组(D组),每组10只。D组适应性喂养7 d后,连续3 d腹腔注射GSH。4组均于10 d后禁食24 h,禁水12 h,用无水乙醇灌胃1 h后,A组不受+Gz作用,B组暴露于+5 Gz值3 min,C、D组暴露于+10 Gz值3 min,下离心机后观察各组胃黏膜损伤情况,并检测胃黏膜中丙二醛(MDA)、GSH的含量及谷胱甘肽过氧化物酶(GSH-Px)的活性。结果各组大鼠胃黏膜在肉眼观察均有损伤,损伤程度:+10Gz值暴露组+5 Gz值暴露组无水乙醇对照组GSH预处理组,B组与A组相比差异均有统计学意义(P均0.05),C组分别与A、B两组相比差异均有统计学意义(P0.05);D组胃黏膜损伤最轻,与C组相比差异有显著统计学意义(P0.01)。与A组相比,B组胃黏膜中MDA、GSH含量变化不明显,差异均无统计学意义(P均0.05),GSH-Px活性明显升高,差异有显著统计学意义(P0.01);与A、B两组相比,C组胃黏膜中MDA含量升高明显,GSH含量降低明显,GSH-Px活性明显降低,差异均有统计学意义(P0.05);与C组相比,D组胃黏膜MDA含量明显降低,GSH的含量明显升高,GSH-Px的活性明显升高,差异有统计学意义(P0.05)。结论 GSH对+Gz值暴露引起的急性胃黏膜损伤大鼠的胃黏膜有预防及保护作用,该作用可能是通过增加胃黏膜GSH的含量、GSH-Px的活性及抑制MDA的作用而实现的。     

谷胱甘肽系统对2型糖尿病患者冠状动脉病变程度的影响

目的探讨谷胱甘肽系统对2型糖尿病(T2DM)患者冠状动脉病变程度的影响。方法选取行冠状动脉造影术的患者236例,分为正常糖耐量(NGT)组126例,T2DM组110例,检测患者的血液生化指标以及还原型谷胱甘肽(GSH)、GSH过氧化物酶(GSH-Px)和谷胱甘肽还原酶(GR)的活性。根据冠状动脉造影结果,采用Gensini评分系统对每支血管病变程度进行定量评分。结果 T2DM组血浆GSH[(3.87±1.55)μg/L vs(4.45±1.94)μg/L]、GSH-Px[(0.29±0.05)ng/L vs(0.35±0.08)ng/L]和GR[(0.19±0.07)ng/L vs(0.26±0.08)ng/L]活性明显低于NGT组,差异有统计学意义(P<0.05)。校正年龄、体重指数、血压、血脂、空腹血糖、空腹胰岛素、餐后2h血糖、餐后2h胰岛素、糖化血红蛋白因素后,T2DM组GSH、GSH-Px、GR活性与Gensini积分呈负相关(P<0.05,P<0.01)。T2DM组GSH、GSH-Px和GR活性对Gensini积分的影响作用最大。结论 T2DM患者血浆GSH、GR和GSH-Px活性的降低与冠状动脉病变程度具有一定的负相关性,且为该人群冠状动脉病变的独立影响因素。     

抗氧化剂对去卵巢大鼠骨密度和血清生化指标的影响

目的 研究抗氧化剂维生素C、E及还原型谷胱甘肽(GSH)不同配伍用药方法对去卵巢大鼠骨密度及血清生化指标的影响.方法 4月龄雌性SD大鼠70只,随机取50只行双侧卵巢切除术,20只行假手术.3个月后随机从手术组和假手术组各取10只大鼠检测体重、子宫湿重、左侧股骨及腰椎骨密度和血清生化指标Ca2+、肌酐、碱性磷酸酶(ALP)水平,以确定骨质疏松模型建立成功.确定模型建立成功后,其余动物分为A(假手术)、B(去卵巢生理盐水对照组)、C(维生素C+维生素E)、D(GSH)、E(维生素C+维生素E十GSH)5组,每组10只.药物用最维牛素C(750 mg·kg-1·d-1)、GSH(125 mg·kg-1·d-1)腹腔注射,维牛素E(250 mg·kg-1·d-1)灌胃,模型组每天以生理盐水腹腔注射.3个月后,检测各组动物左侧股骨及腰椎骨密度和血清生化指标.结果 抗氧化剂治疗3个月后,与模型组相比,左侧股骨及腰椎骨密度三个治疗组均明显增加,其中D、E组增加最显著;血清ALP各组均显著降低;超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)水平和血清抑制OH-能力D、E组显著升高;丙二醛水平C、D组显著降低;各组血清Ca2+水平无明显改变.结论 抗氧化剂维生素C、维生素E及GSH显著增加去卵巢骨质疏松模型大鼠骨密度,阻止血清抗氧化成分(SOD、GSH-Px)减少,提高血清抑制OH-能力,降低脂质过氧化物丙二醛.     

Antioxidant therapy and streptozotocin-induced diabetes in pregnant rats

The aim of our study was to analyse the effect of chronic hyperglycaemia on lipid peroxidation and scavenging enzyme activity in pregnant animals and their offspring supplemented and not supplemented with vitamin E – a natural antioxidant. Thirty pregnant female Wistar rats were used in our experiments. Diabetes was induced on day 7 of pregnancy using a single does of streptozotocin (40 mg/kg). Diabetic animals were divided into two equal groups: vitamin E supplemented and those fed with standard diet. Our controls consisted of 15 healthy rats. On day 1 after delivery homogenates of maternal liver and uterus as well as neonatal lungs and liver were prepared. Then the following parameters were measured: malondialdehyde (MDA) concentrations in the homogenates and blood serum, glutathione (GSH) levels, the activity of CuZn superoxide dismutase (SOD) and glutathione peroxidase (GPx) (Bioxytech, France). Statistical analysis was performed using Mann-Withney U test. The neonates of diabetic rats were smaller than those from healthy rats and serum glucose concentration was markedly higher in diabetic animals, both in mothers and neonates. MDA levels increased significantly, whereas GSH content and SOD as well as GPx activities were markedly diminished in diabetic pregnant rats and their offspring in comparison with the control group. In animals supplemented with tocopherol, MDA concentrations declined significantly, GSH contents and SOD activities were markedly elevated in almost all types of tissues studied, whereas glutathione peroxidase remained suppressed. Our results suggest that diabetic pregnant rats and their neonates are exposed to oxidative stress (OS), but vitamin E supplementation could in part reduce the imbalance between uncontrolled reactive oxygen species generation and scavenging enzyme activity, and may potentially serve as a useful prophylactic factor against OS development: Received: 4 January 1999 / Accepted in revised form: 19 May 1999     

Oxidant/antioxidant status in men with Behçet’s disease

Behçet’s disease (BD) is a chronic, progressive disorder that affects many systems of the body including the eye. The aim of this study was to assess whether the increase in oxidative stress in the affected tissues is reflected by lipid peroxidation and to check for alterations in antioxidants and antioxidant enzyme activities in patients with BD. Erythrocyte antioxidant potential (AOP), glutathione (GSH) and GSH-dependent enzymes (glutathione peroxidase (GSH-Px), glutathione reductase (GRD) and glutathione-S-transferase (GST), catalase (CAT), Cu–Zn superoxide dismutase (Cu–Zn SOD) activities, malondialdehyde (MDA) and some trace elements (zinc, Zn; copper, Cu; manganese, Mn) levels in men with BD. Erythrocyte CAT, GSH-Px activities, MDA, GSH, AOP and serum Zn values were significantly lower in patients with BD than in the control group. However, erythrocyte Cu–Zn SOD, GRD activities, erythrocyte sedimentation rate (ESR), serum C-reactive protein (CRP) and Cu values were significantly higher in patients with BD than in the control group, but GST activity and serum Mn values were unchanged. In conclusion, our results confirm the presence of oxidative stress in patients with BD and suggest that the severity of BD may arise from impaired antioxidant mechanisms. Therapy with antioxidants may lead to the increase in the antioxidant defense system and thus improvement in clinical symptoms.