Brain glutathione reductase induction increases early survival and decreases lipofuscin accumulation in aging frogs

Brain catalase was continuously depleted throughout the life span starting with a large population of initially young and old frogs. Free radical-related parameters were measured in the brain tissue once per year after 2.5, 14.5, and 26.5 months of experimentation. Brain lipofuscin accumulation was observed after 14.5 and 26.5 months, and survival was continuously followed during 33 months. The age of the animal did not decrease endogenous antioxidants nor increase tissue peroxidation either in cross-sectional or longitudinal comparisons. Continuous catalase depletion similarly affected young and old animals, inducing glutathione reductase, tending to decrease oxidized glutathione/reduced glutathione (GSSG/GSH) ratio, decreasing lipofuscin accumulation in the brain, and increasing survival from 46% to 91% after 14.5 months. At 26.5 months of experimentation the loss of the glutathione reductase induction in catalase-depleted animals was accompanied by the presence of higher lipofuscin deposits than in controls and was followed by a great increase in mortality rate. Even though the maximal life span (7 years) was the same in the control and treated animals which were already old (4.2 years) at the beginning of the experiment, the treated animals showed a strong reduction in the rates of early death. It is proposed that the maintenance of a high antioxidant/prooxidant balance in the vertebrate brain greatly increases the probability of the individual to reach the final segments of its species-specific life span. © 1993 Wiley-Liss, Inc.     

Free oxygen radicals in restraint-induced stress gastritis in the rat

In this experimental study, the role of free oxygen radicals (FOR) in stress gastritis (SG) was investigated in a restraint stress model for rats. Allopurinol, dimethyl sulfoxide (DMSO), and superoxide dismutase (SOD) were tested as single agents in controlled groups. The portal blood pH values, the ratio of the mucosal erosion area to the gastric mucosal area (EA/MA), the ratio of the depth of mucosal erosions to the concomitant gastric mucosal wall (ED/MD), and concentrations of malondialdehyde (MDA) — a lipid peroxidation coproduct — in the gastric mucosa were used as parameters in the experiment. The EA/MA between the treated and untreated control groups were found to have no statistically significant difference (P > 0.05). ED/MD, a crucial determinant for bleeding probability, was found to be decreased in the SOD group (P < 0.05). SOD, allopurinol, and DMSO reduced the mucosal MDA concentration to lower values than the untreated group (P < 0.05). We concluded that although FOR may not play a dominant role in stress-induced gastric lesions, SOD may be a good candidate for a clinical trial on SG prophylaxis.     

心可舒对心肌缺血再灌注损伤的保护作用

目的 :探讨心可舒对心肌缺血再灌注损伤的保护作用 ,并初步探讨其作用机制。方法 :19只家兔随机分为 3组 :①假手术组 (SH组 ,n =6 ) :开胸 ,左冠状动脉前降支 (LAD)只穿线不结扎 ,旷置 2 0min ,再观察 6h ;②缺血 再灌注组 (IR组 ,n =7) ;③心可舒处理组 (XKS组 ,n =6 ) :两组均开胸结扎兔LAD 2 0min ,然后松扎 6h。以电镜下心肌超微结构、心率、再灌注心律失常、左室功能、右室血清SOD活性和MDA的含量及心肌组织中SOD、MDA、ATP水平为观察指标。结果 :3组心率均呈进行性下降趋势 ,其中IR组下降幅度最大。XKS组左室内压力上升和下降速率及左室内压峰值均显著高于IR组 (P <0 .0 1) ,血清及心肌组织中SOD活性和心肌组织中ATP含量显著高于IR组 (P <0 .0 1) ,而MDA含量显著低于IR组 (P <0 .0 1) ,再灌注心律失常发生率低于IR组 (P <0 .0 1) ,XKS组心肌超微结构损害较轻。与SH组比较 ,XKS组上述各指标均无显著差异 (P >0 .0 5 )。结论 :心可舒可促进心肌缺血 再灌注损伤心功能的恢复 ,其作用机制可能与清除氧自由基、改善心肌能量代谢等有关。     

Ginkgo biloba modulates glutathione redox cycle in vascular endothelial cells

We recently reported that Ginkgo biloba extract (GBE) suppressed oxidative burst in macrophages and protected bovine pulmonary artery endothelial cells (PAEC) from oxidant injury. In this study the effects of GBE on glutathione (GSH) redox cycle and activity of antioxidant enzymes were investigated. Confluent monolayers of PAEC were incubated with GBE for 8–48 h, washed, and then lysed with Triton X-100. Biochemical assays were performed with the lysate. GBE caused both dose- and time-dependent increase in GSH level and glutathione disulfide (GSSG) reductase activity while GSH peroxidase and superoxide dismutase activity remained unaffected. Exposure of PAEC to an organic oxidant tert-butyl hydroperoxide (tBHP) resulted in decreased GSH level, increased lipid peroxidation, and elevated leakage of intracellular lactate dehydrogenase. Preincubation or simultaneous treatment of PAEC with GBE prevented these changes induced by tBHP. Our data suggest that the antioxidant effect of GBE may be due to its modulation of the GSH redox cycle in PAEC as well as direct scavenging of the oxidant.     

柴胡注射液对小鼠灌流肝脏缺氧复氧损伤的保护作用

采用小鼠离体肝灌流术在Krebs－Henseleit（K－H）灌流液中加入柴胡注射液，观察柴胡对肝缺氧（1h）复氧（1h）的影响。结果表明：柴胡组与缺氧组相比，光镜电镜下肝组织损伤较轻，且肝组织乳酸脱氢酶（LDH）漏出量显著减少，脏／体比、还原型谷胱甘肽（GSH）及黄嘌呤氧化酶（XOD）含量有显著性差异，丙二醇（MDA）生成延迟。揭示柴胡对小鼠离体灌流肝缺氧复氧损伤有明显拮抗作用，其机制与抑制氧自由基形成有关。     

热毒清对内毒素所致家兔DIC氧自由基代谢的影响

采用内毒素所致家兔弥散性血管内凝血(DIC)为模型,观察热毒清是否具有抗自由基作用。实验表明,与模型组比较,热毒清组血清、肝匀浆和线粒体LPO含量以及血清和肝匀浆XOD活性均显著降低;而肝匀浆SOD以及肝匀浆和线粒体GSH-Px活性明显升高。结果提示热毒清能有效地拮抗内毒素DIC 病理过程中增多的自由基,并通过抑制自由基生成酶和增强自由基清除酶活性而起作用。从而部分解释了热毒清保护细胞器的作用机理。     

吻合血管尺动脉腕背支为蒂双叶皮瓣的临床应用

目的：探讨尺动脉腕背支为蒂开支与降支分别为营养血管制 双叶游离皮瓣在手指外伤中的应用。方法：9只成人新鲜上肢标本，左4只，右5只，于尺动脉腕背支起始处灌注红色乳胶，手术显微镜下解剖观察尺动脉腕支及其升支与降支起始，行程、分支及吻合情况，临床设计以尺动脉腕背支为蒂，腕背支的升支与降支分别为营养血管的双叶游离皮瓣修复单指皮肤全脱套伤8例，示中指及中环指背或指掌侧皮肤缺损7例。结果：临床应用15例，皮瓣全部成活，术后随访6-15个月，伤指外形及皮肤色质与健指相似，常侧远端指脂两点辨觉为3.2-6.1mm，运动功能按TAM系统标准评价；优6指，良8指，可4指。结论：尺动脉腕背支为蒂升支与降支分别为营养血管的双叶游离皮瓣，是修复单指皮肤全脱套伤及相邻两指背或掌侧皮肤的一种良好方法。     

不同食谱诱发地鼠形成两类不同胆石的实验研究

目的探讨两类不同食谱诱发叙利亚金黄地鼠形成胆石情况。方法采用高糖无脂饲料诱发幼年叙利亚金黄地鼠形成胆固醇结石（ＣＨＳ），用低蛋白高纤维素饲料诱发成年叙利亚金黄地鼠形成胆色素结石（ＰＳ）。结果６周后两组动物的成石率分别为７０．１％和８０．０％，死亡率分别为１５％和０，其结石的胆固醇含量分别为９２％±４．７％和１７％±３．８％。结论叙利亚金黄地鼠是研究两类胆石形成的良好实验动物之一。     

Studies on the Relationship between Production of Oxygen Free Radicals and Cardiac Failure of Coronary Artery Disease

<正> In this paper, the relationship between Oxygen Free Radicals（OFR） and cardiac failure of Coronary Artery Disease（CAD）was studied. The authors analyse the release of OFR, as measured by Lumin-dependent chemiluminescence, from the polymorphonuclear leukocytes（PMN）; the activity of plasma superoxide dismutase （SOD） and the concentration of malondialdehyde（MDA）in patients of CAD with heart failure. The results showed that compared with the health controls and the group of CAD without heart failure, the release of OFR in respiratory burst of the PMN stimulated with PMA（phorbol myristate acetate）and the concentration of MDA in plasma were significantly increased（p<0.05） and the activity of SOD was markedly lower（p<0.05）in the group of CAD with heart failure.It suggests that the enhanced production of OFR by PMN, the increased concen tration MDA in plasma and the decreased SOD might be associated with the genesis and development of cardiac failure, The use of agents that reduce the amount of OFR would be of value in the prevention and treatment of cardiac failure.     

Superoxide dismutase partially prevents sympathetic denervation by 6-hydroxydopamine

Summary The effects of superoxide dismutase (S.O.D.) in two models of chemical denervation induced by 6-hydroxydopamine (6-OHDA) were studied.To evaluate the effects of S.O.D. on in vitro 6-OHDA-induced denervation, fragments of the lateral saphenous veins of mongrel dogs were pre-incubated in oxygenated Krebs-Henseleit solution with or without S.O.D. and then incubated under control conditions, with 6-OHDA or with 6-OHDA + S.O.D. Following the incubation period the fragments were repeatedly washed with Krebs solution and then used for determination of noradrenaline and for morphological study. 6-OHDA produced a profound depletion of noradrenaline. This depletion was significantly reduced although not prevented by S.O.D. The protective effect of S.O.D. was concentration-dependent. The ultrastructural study confirmed the 6-OHDA-induced sympathetic nerve degeneration as well as the protective effect afforded by S.O.D.In order to evaluate the effects of S.O.D. on in vivo 6-OHDA-induced denervation, male Wistar rats were anaesthetized and the tail vein cannulated. Saline or S.O.D. were intravenously delivered. 6-OHDA was injected five minutes after the beginning of infusions. Fragments of the left ventricle and vasa deferentia were used for determination of noradrenaline and for morphological study. 6-OHDA produced a significant depletion of noradrenaline in the left ventricle and vas deferens (to 8% and 18% of control values respectively). This depletion was reduced, though not prevented by S.O.D. Morphological data confirmed the neurotoxic effect of 6-OHDA and a protective role for S.O.D.In the concentration shown to afford protection against in vitro 6-OHDA-induced denervation, S.O.D. neither chemically inactivated 6-OHDA, nor did it exert any blocking effect on the neuronal uptake of ³H-noradrenaline. Thus, the protection afforded by S.O.D. against chemical denervation by 6-OHDA appears to be due to the free radical scavenging effect of S.O.D. Send offprint requests to A. Albino-Teixeira at the above address