苷糖酯对脂质过氧化损伤红细胞变形能力的膜收缩蛋白变化？…

①目的 观察甘糖酯（ＰＧＭＳ）对脂质过氧化损伤红细胞变形能力和膜收缩蛋白的影响,探讨其保护红细胞的机制。②方法 以黄嘌呤氧化酶（ＨＸＯ）氧自由基体系和活性氧（Ｈ２Ｏ２）作用于红细胞,观察ＰＧＭＳ对红细胞溶血度、红细胞膜脂质过氧化物（ＬＰＯ）、红细胞变形能力（ＥＤ）、红细胞收缩蛋白二聚体（ＳＰ－Ｄ）和四聚体（ＳＰ－Ｔ）的影响。③结果 ＰＧＭＳ能明显降低红细胞溶血度,与对照组比较差异有极显著性ｔ＝３．     

卡托普利对自发性高血压大鼠血压及其靶器官脂质过氧化作用的影响

用卡托普利治疗自发性高血压大鼠（ＳＨＲ），观察大鼠血压以及靶器官心、脑、肾组织脂质过氧化产物丙二醛（ＭＤＡ）含量及锰－超氧化物歧化酶（Ｍｎ－ＳＯＤ）活力的改变。结果表明，ＳＨＲ心、脑、肾组织ＭＤＡ含量增加，且Ｍｎ－ＳＯＤ活力增强，存在严重的脂质过氧化损伤。卡托普利对ＳＨＲ有显著的降压作用和减轻靶器官脂质过氧化损伤作用。     

芸香甙抗氧化作用的初步研究

芸香甙（Ｒｕ）是黄酮类化合物，本文就其抗氧化作用进行研究。在兔ＲＢＣ体外温育自氧化试验中，３．２×１０－５ｍｏｌ·Ｌ－１Ｒｕ可显著抑制ＲＢＣ自氧化．并可减少ＲＢＣ自氧化过程中脂质过氧化产物──ＭＤＡ的含量．说明ＲＵ对ＲＢＣ的自氧化溶血损伤有一定的保护作用，并可能与抑制脂质过氧化反应有关；灌胃Ｒｕ２０～８０ｍｇ·ｋｇ－１不仅可显著减少小鼠血浆中ＭＤＡ含量，也可显著提高大鼠血浆中ＳＯＤ活性，并有一定的量效关系，结果进一步提示ＲＵ抗脂质过氧化作用可能与提高ＳＯＤ活性有关。     

非创伤性下肢缺血预处理对大鼠缺血再灌注心肌脂质过氧化的保护作用

采用非创伤性下肢缺血预处理（Ｎ－ＷＩＰＣ）动物模型,研究了Ｎ－ＷＩＰＣ对大鼠心肌缺血再灌注损伤及脂质过氧化的保护效应。结果显示,Ｎ－ＷＩＰＣ可明显减少心肌组织内肌酸磷酸激酶（ＣＰＫ）的漏出,提高心肌组织超氧化物歧化酶（ＳＯＤ）的活性,降低脂质过氧化产物丙二醛（ＭＤＡ）的含量。表明非创伤性下肢缺血预处理具有抗心肌缺血再灌注损伤及脂质过氧化的作用,其机制可能是通过提高内源性心肌保护物质的水平而起作用。     

脑再灌注损伤及东菱克栓酶的保护作用

用Ｗｉｓｔａｒ大鼠４条血管关闭的全脑缺血再灌注模型，观察脑缺血再灌注脑组织超氧化物歧化酶（ＳＯＤ）活性及丙二醛（ＭＤＡ）含量的变化及东菱克栓酶对它的影响。发现对照组脑组织ＭＤＡ含量及ＳＯＤ活性均高于假手术组的ＭＤＡ含量及ＳＯＤ活性，Ｐ〈０．０１及〈０．００１，而东菱克栓酶组的ＭＤＡ含量显著低于对照组与对照组间的差异不显著，提示东菱克栓酶具有清除自由基、抗脂质过氧化作用。     

钙通道阻滞剂抗肝缺血—再灌注损伤作用机制的实验研究

目的 探讨钙通道阻滞剂（ＣＣＥＢ）对肝缺血一再灌注损伤（ＨＩＲＩ）防治作用的机制。方法制备家兔ＨＩＲＩ模型,动态观察维拉帕米（ＶＰ）和地尔硫卓（ＤＴ）对肝组织及血中黄嘌呤氧化酶（ＸＯ）、超氧化物歧化酶（ＳＯＤ）活性及脂质过氧化物（ＬＰＯ）浓度的影响。结果 ＶＰ组和ＤＴ组ＯＸ活性及ＭＤＡ含量分别显著低于对照组（均Ｐ＜０．０１）,而ＳＯＤ活性与对照组比较均无显著性差异（均 Ｐ＞ ０．０５）。结论 ＣＣＥＢ抗 ＨＩＲＩ的机制与其降低 ＸＯ活性、抑制脂质过氧化反应密切相关。     

克罗卡林对心肌细胞脂质过氧化作用的实验研究

在细胞水平研究克罗卡林缺氧再给氧时对细胞内丙二醛（ＭＤＡ）含量，超氧化物歧化酶（ＳＯＤ）活性及细胞膜脂质流动性的影响，探讨克罗卡林克抗脂质过氧化作用及其可能机制。     

3，6—（二甲氨基）—二苯并碘杂六环柠檬酸盐保护大鼠缺血再灌注心肌与抗脂质过氧化的关系

在大鼠在体心肌缺血再灌注模型上，观察了３、６（二甲氨基）二笨并碘杂六环柠檬酸盐（１６５）的抗心肌缺血再灌注损伤及抗脂质过氧化作用结果表明１－６５能明显改善缺血再灌注所致的心肌光镜及电镜下细胞结构损伤，升高心肌超氧化物歧化酶和谷胱甘肽过氧化物酶活性，减少丙二醛生成提示Ｉ６５对心肌缺血再灌注损伤的保护作用与保护氧自由基清除酶的活性．防止膜脂质过氧化有关     

山莨菪碱对心肌缺血再灌注损伤的作用与抗脂质过氧化

研究山莨菪碱对心肌缺血再灌注损伤的作用与抗脂质过氧化的关系。方法：在麻醉大鼠心肌缺血１５ｍｉｎ再灌注１０ｍｉｎ模型上，于再灌注前１ｍｉｎｉｖ山莨菪碱（Ａｎｉ）１，３，５ｍｇ．ｋｇ＾－１，结果：减少心肌ＣＫ的释放和ＭＤＡ含量的升高，保持ＳＯＤ活性，并完全阻止再灌注心肌膜中油酸，亚油酸和花生四烯酸的减少，ＳＯＤ７５Ｕ．ｋｇ＾－１的作用与Ａｎｉ３ｍｇ．ｋｇ＾－１相当。结论：Ａｎｉ的抗脂质过氧化可能是其保     

解酒灵对乙醇致鼠肝急性损伤的保护作用及机制的探讨

目的：探讨解酒灵解酒作用的机制。方法：利用自动生化分析仪、ＴＢＡ显色法、邻苯三酚自氧化法分别测定血清中ＡＬＴ和ＡＳＴ活性及肝匀浆中丙二醛（ＭＤＡ）和超氧化物歧化酶（ＳＯＤ）活性;用ＨＥ染色法、ＰＡＳ染色法观察肝组织形态学的病变。结果：解酒灵能抑制乙醇所致的ＡＬＴ和ＡＳＴ活性的升高和脂质过氧化物的升高（Ｐ〈０．０１）,能诱变ＳＯＤ活性。结论：解酒灵对乙醇所致鼠肝急性损伤的保护作用机制与抗自由基的产生     

Chrysotile Inhibits Glutathione-Dependent Protection against the Onset of Lipid Peroxidation in Rat Lung Microsomes

Abstract: The glutathione and vitamin E-dependent protection of lipid peroxidation in an NADPH (0.4 mM) and chrysotile (500 μg/ml) containing system were investigated in vitro in rat lung microsomes. Addition of 1 mM glutathione to the above reaction system containing microsomes supplemented with vitamin E (1 nmol/mg protein) reduced lipid peroxidation. Similar protection by glutathione could be observed in normal unsupplemented microsomes though the degree of protection was less pronounced. Addition of free radical scavengers such as, superoxide dismutase (100 units/ml), catalase (150 units/ml), mannitol (1 mM) and β-carotene (0.5 mM) to the reaction system showed an insignificant effect on lipid peroxidation. When the reaction was carried out in absence of glutathione, vitamin E content of peroxidizing microsomes decreased rapidly. In this system a concomitant increase in the activity of microsomal glutathione-S-transferase was observed which may serve as an alternative pathway to detoxify lipid peroxides. Addition of glutathione alone to the reaction system prevented both against the loss in vitamin E content and increase in the activity of glutathione-S-transferase. Supplementation of both vitamin E and glutathione was found to be effective in lowering glutathione-S-transferase activity to that of normal basal level. Our results suggest that chrysotile-mediated stimulation of NADPH-dependent lipid peroxidation may be due to hampering of glutathione-dependent protection which may ultimately exhaust membrane bound vitamin E. Our data further suggest that the lung tissue may have an inbuilt mechanism whereby glutathione-S-transferase may be triggered to cope with the excessive production of lipid peroxides.     

Effect of dimethyl sulfoxide on gentamicin-induced nephrotoxicity in rats

Nephrotoxicity of gentamicin (GM) has been suggested to be mediated by the generation of reduced oxygen metabolites. The present study investigated the possible protective role of the free radical scavenger dimethyl sulfoxide (DMSO) on some indices of GM nephrotoxicity in rats. The antibiotic was injected intramuscularly (i.m.) at a dose of 100 mg/kg for six consecutive days, either with or without treatment with DMSO (12.5%, 25% or 50% in saline) at an intraperitoneal (i.p.) dose of 2 ml/kg 4 days before GM, and concomitantly with GM treatment thereafter. DMSO (25% in saline) was also given as above to rats treated with GM at i.m. doses of 25, 50 or 100 mg/kg for six consecutive days. GM caused dose-dependent significant increases in the concentrations of urea and creatinine in plasma, and in thiobarbituric acid reactive substances (TBARS) level in the kidney cortex and also caused significant decreases in the concentrations of reduced glutathione (GSH) and superoxide dismutase (SOD) activity. In GM-treated rats, DMSO dose-dependently lowered the elevated plasma urea and creatinine concentrations, and the rise in cortical TBARS. It also restored the levels of GSH and SOD activity to near normal. DMSO (25%) was effective in completely preventing the development of signs of nephrotoxicity of G (50 mg/kg). Treatment of the rats with DMSO alone, at any of the above doses, did not alter significantly any of the renal or hepatic function tests studied, and did not appear to adversely affect the kidney or liver histology. However, the efficacy and safety of DMSO require further studies. It is suggested that DMSO has potential protective effect against GM nephrotoxicity in rats.     

Activation of the microsomal glutathione-S-transferase and reduction of the glutathione dependent protection against lipid peroxidation by acrolein

Allyl alcohol is hepatotoxic. It is generally believed that acrolein, generated out of allyl alcohol by cytosolic alcohol dehydrogenase, is responsible for this toxicity. The effect of acrolein in vitro and in vivo on the glutathione (GSH) dependent protection of liver microsomes against lipid peroxidation, and on the microsomal GSH-S-transferase (GSH-tr) in the rat was determined. In vitro incubation of liver microsomes with 5 mM acrolein for 30 sec resulted in a 2-fold activation of the GSH-tr. This activation probably proceeds via alkylation of the thiol group of the GSH-tr. In vivo administration of 1.1 mmol allyl alcohol/kg to rats did also result in a 2-fold stimulation of the GSH-tr activity. Administration of 375 mg pyrazole/kg, an inhibitor of the alcohol dehydrogenase, thus reducing the acrolein formation, prevented the in vivo stimulation of GSH-tr by allyl alcohol. This indicates that the activation of GSH-tr in vivo by allyl alcohol probably also proceeds via alkylation of the thiol group of the GSH-tr by acrolein. GSH protects liver microsomes against lipid peroxidation, probably via a free radical reductase that reduces vitamin E radicals at the expense of GSH. Incubating liver microsomes for 30 min with 0.1 mM acrolein reduced the GSH dependent protection against lipid peroxidation, probably because an essential thiol group(s) on the free radical reductase is alkylated. In vivo administration of allyl alcohol did not reduce the GSH dependent protection of the microsomes. Probably the thiol group(s) located on the free radical reductase is less accessible or less reactive than the thiol group on the GSH-tr. After administration of allyl alcohol we found no evidence for in vivo lipid peroxidation. Therefore we could not evaluate the importance of the GSH dependent protection against lipid peroxidation in vivo.     

黄芪活性成分对膜损伤的防护作用

目的　了解黄芪活性成分对人体细胞膜损伤的防护作用。方法　采用 2种活性氧产生体系诱发膜脂质过氧化为实验模型 ,观察了黄芪活性提取成分对膜脂质过氧化作用的防护效能。结果　黄芪活性提取成分对多种自由基均有良好的清除作用 ,其中黄芪总黄酮和黄芪总皂甙的作用最佳。结论　黄芪的活性成分对氧自由基造成的细胞膜损伤具有明显的防护作用。     

Extracts from dulse (Palmaria palmata) are effective antioxidants and inhibitors of cell proliferation in vitro.

Previously, we reported that a 1-butanol soluble extract of the edible red alga Palmaria palmata, known as dulse, exhibited hydroxyl and stable free radical scavenging activity as well as inhibition of lipid peroxidation, attributed to the reducing activity and polyphenol content of the dulse extract. In the present study, we evaluated the antioxidant and antiproliferative activities of two grades of dulse harvested from Canadian Maritime locations differing in UV radiation exposure (i.e. west versus east coasts of Grand Manan Island, New Brunswick). The 1-butanol soluble extract from Grade 1 dulse (reduced UV-exposure) exhibited lower reducing activity versus Grade 2 dulse (greater UV exposure) reflecting a lower requirement for endogenous antioxidant protection. Grade 1 and 2 dulse extracts both inhibited (p0.03) AAPH-induced lipid peroxidation, but had no effect on AMVN-induced lipid peroxidation, demonstrating the aqueous nature of the antioxidants involved. The Grade 1 and 2 dulse extract inhibition (p<0.05) of HeLa cell proliferation was dose-dependent over 0.5-5.0mg/mL and maximal at 48 and 72h incubation. The antiproliferative effects of the Grade 1 and 2 dulse extracts in the present study likely reflect the bioactivity of the polyphenol content of these extracts.     

In vitro anti-oxidant and DNA protective effects of the novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor rosuvastatin

1. Free radical-induced lipid peroxidation and changes in protein and nucleic acid structures can result in various human ailments, including ageing, neurodegenerative disorders and cancer. High body fat or dietary fat further enhances the free radical-mediated pathogenesis of various diseases. 2. In the present study, the in vitro anti-oxidant and DNA protective effects of the novel cardiovascular drug rosuvastatin were evaluated. Anti-oxidant activity was evaluated on the basis of inhibition of lipid peroxidation, scavenging of superoxide radical and the reduction of ferric ions (Fe(3+)). Inhibition of lipid peroxidation was determined using Fenton's reaction-induced lipid peroxidation in rat liver and brain homogenates and liver mitochondria. Superoxide radical-scavenging activity was evaluated by scavenging of the superoxide anion generated by photo illumination of riboflavin and Fe(3+)-reducing activity was determined by the ferric-reducing anti-oxidant power (FRAP) assay. DNA protection was evaluated according to changes in H(2)O(2)-induced pBR322 plasmid DNA and Fenton's reaction-induced-fragmentation of rat liver DNA. 3. The results indicate that rosuvastatin (1.5 or 2 mg/mL) is able to protect against lipid peroxidation. Furthermore, H(2)O(2)-induced changes in pBR322 plasmid DNA and fragmentation of hepatic DNA were alleviated by rosuvastatin. However, rosuvastatin did not show any superoxide anion-scavenging activity. The protective mechanism of rosuvastatin can be correlated with the reducing equivalent donating property or direct hydroxyl radical-scavenging activity of the drug. 4. The pleiotropic activities of rosuvastatin exhibited suggest its clinical advantages against oxidative stress-induced human ailments in addition to its widely using hypolipidaemic effect.     

丹酚酸B镁盐对自由基的清除作用和对脂质过氧化的抑制作用(英文)

AIM: To study the effect of magnesium lithospermate B (MLB) on the lipid peroxidation and on its free radical scavenging activity. METHODS: MLB was incubated in rat tissue homogenate or in a free radical generating system. MLB induced inhibition of lipid peroxidation and its scavenging activity on superoxide anions and hydroxyl radicals was studied using colorimetric estimation. RESULTS: MLB inhibited the lipid peroxidation induced by either an auto-oxidant or Fe2+/VitC in vitro, in the liver homogenate, the inhibitory rate of MLB (10 mg/L) being 69.2% and 57.7%, respectively. MLB (25 and 50 mg/kg) decreased the amount of thiobarbituric acid reactive substances (TBARS) in rat serum, liver, kidney, and heart. However, it did not inhibit the lipid peroxidation of brain homogenate ex vivo. MLB scavenged superoxide anions generated from xanthine/xanthine oxidase system and iron-dependent hydroxyl radicals. CONCLUSION: MLB is an inhibitor of lipid peroxidation and scavenge superoxide anions and hydroxyl radicals both in vitro and ex vivo.     

褪黑素拮抗鼠肝线粒体自由基产生的实验研究

目的观察褪黑素拮抗氧自由基和对膜脂质过氧化损伤的保护作用。方法用电子自旋共振技术，以ＤＭＰＯ和４－ＰＯＢＮ为捕集剂，捕集Ｆｅｎｔｏｎ反应产生的羟自由基和Ｆｅ２＋启动的鼠肝线粒体膜脂质过氧化产生的脂类自由基，以脂肪酸自旋标记物５－Ｄｏｘｙｌ和１６－Ｄｏｘｙｌ标记线粒体膜，研究脂质过氧化损伤后膜流动性的变化。结果褪黑素对羟自由基和脂类自由基有良好的清除作用，５０％清除浓度分别为１８６μｍｏｌ·Ｌ－１和４５０μｍｏｌ·Ｌ－１，而且在５００μｍｏｌ·Ｌ－１浓度范围内能防止脂质过氧化引起的线粒体膜流动性降低。结论褪黑素是一个有效的抗氧化剂，能防止生物膜的脂质过氧化损伤。     

Antioxidant properties of the alkaloid boldine in systems undergoing lipid peroxidation and enzyme inactivation

Boldine, in low micromolar concentrations, was able to prevent brain homogenate autooxidation, the 2,2'-azobis(2-amidinopropane)(AAP)-induced lipid peroxidation of red cell plasma membranes, and the AAP-induced inactivation of lysozyme. These results are indicative of a high reactivity of boldine towards free radicals. The analysis of the boldine effect as a function of incubation times suggests that a metabolite resulting from the interaction of boldine with free radicals also exhibits antioxidant activity, being more efficient than boldine in brain homogenate auto-oxidation and less efficient in lysozyme protection experiments. This behavior may be accounted for in terms of the relative location of the scavengers needed to afford maximal protection.