栀子苷体外抗氧化作用

目的探讨栀子苷的体外抗氧化作用。方法采用羟自由基和脂质过氧化体系,研究栀子苷(0.5,1,2,4,8 g.L-1)对自由基的清除能力和对小鼠肝、肾、心组织匀浆的脂质过氧化抑制作用。结果栀子苷对羟自由基有清除能力,对小鼠肝、肾、心组织匀浆有脂质过氧化抑制作用。结论栀子苷有体外抗氧化能力。     

白花前胡香豆素组分体外抗氧化活性研究

目的 观察白花前胡香豆素组分（TCP）对氧自由基的清除作用及其对脂质过氧化反应的抑制作用。方法羟自由基由Fenton反应体系产生,超氧阴离子自由基由邻苯三酚自氧化法产生,采用硫代巴比妥酸法测定肝匀浆丙二醛（MDA）相对含量来反映TCP对脂质过氧化的影响。结果TCP对羟自由基和超氧阴离子自由基有较强的清除作用,达到50%清除率所需药物浓度（EC50）分别为287.1和124.8 μg•mL 1,并抑制小鼠肝匀浆脂质过氧化反应,EC50为409.5 μg•mL 1。结论TCP对氧自由基有清除作用,并抑制脂质过氧化反应,其活性与剂量呈正相关。     

异莲心碱的体外抗氧化活性

目的研究异莲心碱对氧自由基的清除作用及其对脂质过氧化反应(LPO)的抑制作用。方法羟自由基由Fenton体系产生,超氧阴离子自由基由邻苯三酚自氧化法产生,通过比色法测定LPO的终产物 丙二醛(MDA)的相对含量来反映异莲心碱对LPO的影响。结果异莲心碱对羟自由基和超氧阴离子自由基有较强的清除作用,达到5 0 %清除率所需药物浓度(EC50 )分别为0 .90 ,1.82mg/ml,可抑制小鼠肝匀浆脂质过氧化反应,EC50 为0 .6 7mg/ml。结论异莲心碱对氧自由基有清除作用,对脂质过氧化有抑制作用,其活性与剂量呈正相关     

硒对过氧化氢所致老龄大鼠红细胞溶血及脂质过氧化的影响

本实验给老龄Wistar雄性大鼠腹腔注射亚硒酸钠(30μg/kg)15d,观察硒对过氧化氢所致红细胞溶血及脂质过氧化的抑制作用。结果表明硒降低了过氧化氢对红细胞的溶血率,同时过氧化氢所致脂质过氧化作用明显减弱。     

番木瓜的抗氧化作用研究

目的探讨番木瓜的抗氧化作用。方法红细胞溶血、肝匀浆MDA生成及羟自由基生成用比色法测定,超氧化物歧化酶活力用羟胺法测定。结果番木瓜提取液体外给药能明显抑制H2O2所致红细胞溶血,并抑制小鼠肝匀浆自发性或Fe2 -V itC诱发的脂质过氧化反应。对H2O2所产生的羟自由基亦有直接的清除作用,并可提高大鼠血浆超氧化物歧化酶活力。结论番木瓜具有抗氧化作用。     

马齿苋多糖的抗氧化活性研究

目的研究马齿苋多糖(POP)的抗氧化作用。方法采用体外实验研究POP对超氧阴离子、羟自由基、DPPH的清除作用以及对H2O2诱导的红细胞氧化溶血和大鼠肝匀浆脂质过氧化的保护作用。结果 POP对超氧阴离子和羟自由基具有良好的清除作用,IC50分别为4.29和1.97μg/mL,对有机自由基DPPH的作用很弱。POP对自发性脂质过氧化和H2O2诱导的脂质过氧化具有良好的保护作用,但对H2O2诱导的红细胞氧化溶血作用较弱。结论 POP具有显著的体外抗氧化活性。     

丹参注射液抗羟自由基作用的实验研究

本利用脱氧核糖法测定羟自由基观察到丹参注射液0．67mg／ml可以显抑制小鼠心、肝组织匀浆脂质过氧化作用。结果表明．丹参浓度在1．87mg／ml时抑制羟自由基产生率为30％。     

姜黄素对羟自由基及红细胞氧化性溶血的影响

目：探讨姜黄素（Ｃurcumin,Cur)清除羟自由基及防御脂质过氧化的能力。方法;利用Ｆenton反应生成羟自由基（OH）,由AAPH诱发红细胞氧化性溶血。结果：姜黄素对羟自由基有较强的清除作用（SC50为58．8μmol/L),其作用超过OH的特异性清除剂甘露醇（SC50为2．3μmol/L）;姜黄素（120μmol/L)能有效地抑制由AAPH诱发的红细胞氧化性溶血（抑制2h以上）,显示了较强的防御脂质过氧化的能力。结论：姜黄素对癌症及炎症等的治疗作用可能与其清除自由基及防御脂质过氧化的能力有关。     

番木瓜的抗氧化作用研究

目的探讨番木瓜的抗氧化作用。方法红细胞溶血、肝匀浆MDA生成及羟自由基生成用比色法测定,超氧化物歧化酶活力用羟胺法测定。结果番木瓜提取液体外给药能明显抑制H₂O₂所致红细胞溶血,并抑制小鼠肝匀浆自发性或Fe²⁺-V itC诱发的脂质过氧化反应。对H₂O₂所产生的羟自由基亦有直接的清除作用,并可提高大鼠血浆超氧化物歧化酶活力。结论番木瓜具有抗氧化作用。     

青心酮的抗氧化作用

本文以活性氧对红细胞的氧化作用,探讨青心酮的抗氧化作用。体外实验表明,青心酮有抗超氧化物阴离子自由基及羟基自由基对Hb的氧化作用;减少羟基自由基及过氧化氢引起红细胞溶血和脂质过氧化反应。并发现青心酮有清除超氧化物阴离子自由基及羟基自由基的功能,阻止活性氧对红细胞氧化。     

北极放线菌T-2-3胞外多糖体外抗氧化作用研究

为找外源性的自由基清除剂和抗氧化剂,课题对北极放线菌T-2-3胞外多糖(Arctic Streptomyces sp.extracellular polysaccharide,ASEP)的抗氧化能力进行了研究。通过测定总还原能力(T-AOC)、亚铁离子鳌合能力、超氧阴离子自由基(O2-.)清除能力、羟基自由基(.OH)清除能力和H2O2清除能力,对ASEP和进一步分离组分ASEP-3进行了抗氧化活性初步评价。此外,体外检测了ASEP和ASEP-3对.OH诱导的小鼠肝线粒体MDA生成影响,对H2O2引起的小鼠红细胞溶血的抑制作用及对.OH诱导的肝线粒体肿胀程度的影响。结果显示,ASEP具有一定的抗氧化活性,当ASEP和ASEP-3浓度为200μg/mL时,其对.OH的清除作用分别达到58.0%和99.5%,对O2-.的清除作用达到38.9%和74.2%,对H2O2的清除作用达到12.1%和20.4%,对H2O2引起的氧化溶血的抑制作用达到10.2%和22.8%,对小鼠肝线粒体脂质过氧化的保护作用达到7.9%和14.5%,均呈一定的量效关系,表明ASEP具有一定的抗氧化作用。     

用气相色谱研究抗氧化剂对膜脂肪酸的保护作用

本文应用气相色谱技术直接测定三种生物膜(人红细胞膜,人血小板膜和鼠肝线粒体膜)多不饱和脂肪酸的含量变化,检测脂质过氧化程度。实验证实几种多羟酚类化合物(儿茶精,阿魏酸钠和没食子酸及其衍生物)不同程度地抑制(OH)诱导的脂质过氧化反应,并呈量效和构效关系。这类抗氧化剂对保护生物膜的结构与功能是有益的。     

Copper-induced lipid peroxidation and hemolysis in whole blood: evidence for a lack of correlation

In order to establish a possible relationship between hemolytic and peroxidant activities of copper ions, lipid peroxidation was studied in plasma and whole blood incubated for 24 h with different concentrations of copper. The lipid peroxidation was investigated by the determination of thiobarbituric acid-reactive species, conjugated dienes and fluorescent lipid chromophores. The copper-induced lipoperoxidation was clearly demonstrated in plasma incubated with high concentrations of copper (12.10(-4) and 20.10(-4) M); in whole blood, all the lipoperoxidation products were increased in the plasma, while the fluorescent lipid chromophores remained unchanged in red cells. With a copper concentration similar to that found in acute copper intoxication (4.10(-4) M) no lipoperoxidation was observed and yet hemolysis occurred, reduced glutathione (GSH) decreased dramatically and methemoglobin (MetHb) increased. From these results, we assume that, despite its prooxidant activity and its capacity to produce lipoperoxidation, it has not been proven that copper ions at pathophysiological concentrations induce hemolysis by an oxidative mechanism.     

NADPH-dependent microsomal lipid peroxidation and the problem of pathological action at a distance. New data on induction of red cell damage.

Lipid peroxidation occurs in vitro in a system consisting of rat liver microsomes and NADPH. If a small quantity of red cells is added, they will hemolyze. Lipid peroxidation (i.e. malonic dialdehyde evolution) always precedes red cell hemolysis in our system. This finding is contrary to earlier experiments of others, in which much higher concentrations of red cells were used, and in which certain other conditions varied from those used in our work. Addition of EDTA, which prevented lipid peroxidation, completely prevented red cell hemolysis. When aminopyrine was added, there was vigorous production of formaldehyde and neither lipid peroxidation nor red cell hemolysis occurred. Neither malonic dialdehyde nor hydrogen peroxide is responsible for the red cell hemolysis. If EDTA and erythrocytes are added to a microsomal system that has a prior history of NADPH-induced lipid peroxidation, the erythrocytes show prelytic damage, which can be detected by an osmotic fragility test. If erythrocytes are added to a system in which microsomal lipid peroxidation has been prevented (by the presence of EDTA), there is no evidence of osmotic fragility. These experiments suggest that some product or products arising in the peroxidizing microsomal lipids are capable of producing red cell damage.     

Role of red cell membrane lipid peroxidation in hemolysis due to phenylhydrazine

Although red cell membrane lipid peroxidation has been identified as a consequence of certain oxidizing hemolytic drugs, the relative contribution of lipid peroxidation to red cell damage leading to hemolysis is unclear. This has been evaluated by studying the response to phenylhydrazine of vitamin E-deficient rats as compared to vitamin E-supplemented rats. Following repetitive phenylhydrazinc injections, a lower hematocrit was observed in the vitamin E-deficient group which was associated with higher levels of lipid peroxidation, as indicated by the fluorescence of lipid-containing red cell extracts. However, no significant difference in the initial extent of hemolysis following phenyl-hydrazine injection was observed. Evidence was also obtained suggesting that malonaldehyde, a decomposition product of polyunsaturated fatty acids, is capable of cross-linking hemoglobin to the red cell membrane. These findings suggest that red cell membrane lipid peroxidation is of relatively minor consequence in the acute response to phenylhydrazine but may be of importance in chronic hemolysis due to this oxidizing drug.     

风轮菜活性部位体外抗氧化作用的实验研究

目的研究风轮菜活性部位(CCE)的体外抗氧化活性,为将其开发为新的抗氧化药物提供实验依据。方法通过体外实验测定CCE对超氧阴离子(O-2)、羟基自由基(.OH)及有机自由基DPPH.的清除作用以及对亚铁离子-维生素C(Fe2+-VitC)诱导的小鼠肝脂质过氧化的影响。建立高浓度葡萄糖损伤人脐静脉内皮细胞(HUVECs)的体外模型,测定CCE对细胞超氧化物歧化酶(SOD)和乳酸脱氢酶(LDH)活性的影响。结果CCE能有效清除O-2、.OH和DPPH自由基,其中.OH的清除力最强,对Fe2+-VitC诱导的肝匀浆脂质过氧化反应有明显的抑制作用,且呈浓度依赖性。此外,CCE能明显提高高糖刺激下内皮细胞中的SOD水平,降低LDH活性。结论CCE具有显著的体外抗氧化活性。     

3,3'-diselenodipropionic acid, an efficient peroxyl radical scavenger and a GPx mimic, protects erythrocytes (RBCs) from AAPH-induced hemolysis

3,3'-diselenodipropionic acid (DSePA), a derivative of selenocystine, has been synthesized and examined for antioxidant activity, glutathione peroxidase (GPx) activity, and cytotoxicity. The effect of DSePA on membrane lipid peroxidation, release of hemoglobin, and intracellular K+ ion as a consequence of erythrocyte (red blood cells or RBCs) oxidation by free radicals generated by 2,2'-azobis(2-amidinopropane) hydrochloride (AAPH) were used to evaluate the antioxidant ability. Lipid peroxidation, hemolysis, and K+ ion loss in RBCs were assessed, respectively, by formation of thiobarbituric acid reactive substances (TBARS), absorbance of hemoglobin at 532 nm and flame photometry. The IC50 values for lipid peroxidation, hemolysis, and K+ ion leakage were 45+/-5, 20+/-2, and 75+/-8 microM, respectively. DSePA treatment prevented the depletion of glutathione (GSH) levels in RBCs from free-radical-induced stress. DSePA is a good peroxyl radical scavenger and the bimolecular rate constant for the reaction of DSePA with a model peroxyl radical, trichloromethyl peroxyl radical (CCl 3O2*), was determined to be 2.7x10(8) M(-1) s(-1) using a pulse radiolysis technique. DSePA shows GPx activity with higher substrate specificity towards peroxides than thiols. The cytotoxicity of DSePA was studied in lymphocytes and EL4 tumor cells and the results showed that DSePA is nontoxic to these cells at the concentrations employed. These results when compared with two well-known selenium compounds, sodium selenite and ebselen, indicated that DSePA, although it shows lesser GPx activity, has higher free radical scavenging ability and lesser toxicity.     

Increased erythrocyte antioxidant status protects against smoking induced hemolysis in moderate smokers

Cigarette smoking is common in societies worldwide and has been identified as injurious to human health. Human red blood cells are important targets for electrophilic and oxidant foreign compounds. In the present study, the possible role of antioxidant status on smoking-induced erythrocyte hemolysis of smokers was studied. Erythrocyte superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, reduced glutathione (GSH) level, erythrocyte membrane lipid peroxidation, total cholesterol and phospholipids were determined. Further, nitrite/nitrate levels (NO(2)/NO(3)) in both plasma and erythrocyte lysate were measured. Results showed increased plasma and erythrocyte membrane lipid peroxidation and nitrite/nitrate levels in smokers. The activities of SOD, CAT and GPx were also increased with reduced glutathione (GSH) level in smokers. No significant change was observed in smokers red cell hemolysis and cholesterol/phospholipid (C/P) ratio compared to controls. Erythrocyte membrane lipid peroxidation was positively correlated with SOD (r = 0.482, p < 0.01) and GPx (r = 0.368, p < 0.018) in smokers. Increased levels of nitrite/nitrate and antioxidant status of erythrocytes might be playing a crucial role in protecting red cell from free radical damage induced by cigarette smoke.