过氧化自由基生成法与消除评价法的研究

利用电子自旋共振仪(ESR)对过氧化自由基的几种生成法进行了研讨。确立了偶氮二异丁腈(AIBN)在二甲基亚砜(DMSO)中的热解反应作为过氧化自由基的发生体系,5,5-二甲基-1-吡咯啉-1-氧化物(DMPO)作为自旋捕捉剂,ESR作为检测仪器,α-Tocopherol作为标准物质的过氧化自由基消除能力评价法。

月桂树叶中具有烷基过氧化自由基清除作用化合物的分离及鉴定

为了寻找安全、经济的具有高活性的天然抗氧化剂,采用生物检测系统,对120种草药和食用植物的多种溶剂提取物的烷基过氧化自由基(ROO·)清除活性进行了检测,通过ROO·细胞毒性对金黄色葡萄球菌209p的存活力,发现月桂树(Laurus nobilis)叶溶于乙醇的部分具有强活性。

运动性内源自由基和脂质过氧化对线粒体氧化磷酸化的影响

线粒体膜富含多不饱和脂肪酸，是脂质过氧化损伤的主要部位。急性运动诱发内源性自由基增多及脂质过氧化反应增强。

基于Fe^(2+)-Ce^(4+)体系的库仑滴定法测定药用油脂的过氧化值

药用油脂作为脂溶性药物的溶媒辅料,常用于维生素E滴丸、脂肪乳注射液等药品的生产,然而受氧气、光照及微生物等影响,油脂中不饱和脂肪酸易氧化生成过氧化自由基,通过链式反应直至油脂彻底酸败[1-2].若人体食用过量的过氧化脂质,可破坏细胞正常结构与生理功能,因此国家标准GB 2716-2018《食品安全国家标准植物油》利用过氧化值(过氧化物相当于碘的质量分数)表示油脂中过氧化物含量,以评价其氧化酸败的程度,同时《中华人民共和国药典》(2020年版)也规定了药用油脂中过氧化值的限度(不超过0.13 g/100 g).

体内外自由基形成的研究及意义

目的 :研究体内外自由基的形成及意义。 方法 :用 TBA-醋酸法检测正常人血清 ,血浆 ,胸腹腔渗、漏出液 ,各细胞提取物及服用西洋参前后的血浆和经过氧化处理后的正常人、糖尿病、高血压、冠心病患者的血清及食用油脂、相应烟雾冷凝油的过氧化脂质 (L PO)含量。 结果 :各细胞均有自由基反应 ,以血小板为最高。血清 L PO明显高于血浆 (P<0 .0 0 1) ,胸腹腔渗出液 L PO明显高于漏出液 (P<0 .0 0 1) ,过氧化处理后的糖尿病、高血压、冠心病患者血清的 L PO明显高于过氧化处理后的正常人血清 L PO(P<0 .0 0 1) ;油脂质量越高 ,L PO含量越低 ,相应的烟雾冷凝油的 L PO是食用油脂的 14.3～ 35 .6倍。 结论 :生物、化学和物理因素均可引起脂质过氧化 ,不管何种因素所致的脂质过氧化 ,其反应过程及其产物 L PO对生物体都有严重的损害作用。

体内外自由基形成的研究及意义

目的研究体内外自由基的形成及意义。方法用TBA-醋酸法检测正常人血清,血浆,胸腹腔渗、漏出液,各细胞提取物及服用西洋参前后的血浆和经过氧化处理后的正常人、糖尿病、高血压、冠心病患者的血清及食用油脂、相应烟雾冷凝油的过氧化脂质(LPO)含量。结果各细胞均有自由基反应,以血小板为最高。血清LPO明显高于血浆(P<0.001),胸腹腔渗出液LPO明显高于漏出液(P<0.001),过氧化处理后的糖尿病、高血压、冠心病患者血清的LPO明显高于过氧化处理后的正常人血清LPO(P<0.001)。油脂质量越高,LPO含量越低,相应的烟雾冷凝油的LPO是食用油脂的14.3～35.6倍。结论生物、化学和物理因素均可引起脂质过氧化,不管何种因素所致的脂质过氧化,其反应过程及其产物LPO对生物体都有严重的损害作用。

四君子汤合金匮肾气汤抗自由基损伤的研究

在采用中医四君子汤合金匮肾气汤对抗被实验诱发的小白鼠自由基损伤时，发现两方合用能明显降低小白鼠肝、肺组织中的过氧化脂质含量，并能提高小白鼠肝、脑、肺组织中的超氧化物歧酶的活力，其抗自由基损伤的疗效与维生素E基本相同。

免角膜碱烧伤后角膜超氧化物歧化酶与电子自旋共振波谱的变化

角膜碱烧伤一直是眼科领域的主要研究课题之一。随着分子生物学的发展,自由基和碱烧伤后病理改变的关系受到了不少学者的关注。利用自由基清除剂或抗氧化剂对动物进行实验性治疗已取得初步效果。但是对烧伤后角膜自由基清除酶——超氧化物歧化酶和角膜电子自旋共振波谱变化的研究尚未见报道。本实验的目的即在这方面做初步探索。材料与方法一、动物模型建立:实验选择新西兰白色家兔,体重2～3公斤,健康无眼病.15％噻胺酮肌注麻醉,每公斤体重15～20mg。取9mm直径滤纸圆片。

艇员疗养时超氧化物岐化酶的水平

目的 了解潜艇艇员疗养时超氧化物岐化酶的量。方法 采用比色分析法检测 2 0例健康对照组及 58例潜艇艇员的总超氧化物岐化酶、锰超氧化物岐化酶、铜锌超氧化物岐化酶的量。结果 潜艇艇员的 T-SOD与对照组比较 ,低于对照组 ,经统计处理 ,t=3 .3 4 5,P<0 .0 1。Mn SOD低于对照组 ,t=3 6.44,P<0 .0 0 1。而 Cu Zn SOD两组比较无意义。结论 潜艇艇员在特殊的环境中 ,可因多种有害因素促使他们体内产生脂质过氧化自由基 。

异鼠李素和槲皮素抗氧化活性研究

目的研究东方肉穗草中的主要黄酮类活性成分异鼠李素和槲皮素的抗氧化活性。方法采用清除DPPH自由基、清除ABTS自由基和抑制体外肝脏线粒体脂质过氧化试验的方法,检测异鼠李素和槲皮素的抗氧化活性。结果异鼠李素和槲皮素有明显的抗氧化活性,呈浓度依赖性效应。在清除DPPH自由基、清除ABTS自由基和抑制体外肝脏线粒体脂质过氧化试验中,异鼠李素的体系终浓度IC50分别为32,14.54,6.67μmol/L。槲皮素的体系终浓度IC50分别为4,3.64,6.67μmol/L。结论异鼠李素和槲皮素有明显的抗氧化活性。相同浓度的槲皮素比异鼠李素清除DPPH自由基、清除ABTS自由基能力更强,而抑制体外肝脏线粒体脂质过氧化能力十分接近。

三氟拉嗪对异丙基肾上腺素性大鼠心肌线粒体损伤的影响

目的：研究三氟拉嗪（ＴＦＰ）对缺血心肌线粒体损伤的影响。方法：采用异丙基肾上腺素性心肌梗塞（ＩＳＰ－ＭＩ，皮下注射ＩＳＰ４０ｍｇ／ｋｇ）为模型，观察了ＴＦＰ对缺血心肌线粒体丙二醛（ＭＤＡ）、膜脂流动性、超氧化物歧化酶（ＳＯＤ）及血清磷酸肌酸激酶（ＣＰＫ）的影响。结果：ＴＦＰ明显减轻ＩＳＰ－ＭＩ后心肌线粒体膜脂流动性及ＳＯＤ活力的降低（Ｐ＜０．０５），并显著减少了血清ＣＰＫ及心肌线粒体ＭＤＡ的升高（Ｐ＜０．０５）。结论：ＴＦＰ能部分对抗ＩＳＰ所致的心肌线粒体损伤，其机制可能与抗脂质过氧化作用有关。

Protective Effects of Tea Polyphenol on Cerebral Ischemia-Reperfusion Injury in Rats and Its Scavenging Oxy-radical and Anticerebral Lipid Peroxidation Effects

AIM To study the protective effects of tea polyphenol (TP) on cerebral ischemia reperfusion injury in rats and its scavenging oxygen free radical(OFR) activities and antilipid peroxidation in vitro . METHODS Cerebral ischemia reperfusion injury was produced by bilateral ligation of the common carotid arteries with vagus nerves and reperfusion for 45 min. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. Superoxide anion (O 2) from xanthine xanthine oxidase system and hydroxyl radical (·OH) from Fe 2+ -H 2O 2 system were determined with spectrophotometry. RESULTS During Cerebral ischemia reperfusion,TP improved the activities of superoxide dismutase ( P 【0 05), GSH peroxidase( P 【0 01) and catalase( P 【0 01), while decreasing the maiondialdchyde content in the brain( P 【0 05) and brain water content ( P 【0 01). Tea polyphenol possessed significantly scavenging effects on ·OH produced by Fenton reaction and O 2 produced by xanthine xanthine oxidase system (the IC 50 were 2 2 mmol·L -1 and 1 9 mmol·L -1 respectively). Tea polyphenol could significant inhibit the lipid peroxidation of cerbral mitochondrial membrane induced by ·OH in a concentration dependent manner. CONCLUSION The results indicate that tea polyphenol could protect the injury on cerebral ischemia reperfusion in rats for OFR, these effects may be related to its scavenging effects on oxygen free radicals and antilipid peroxidant.

颈动脉输注高渗透脱水剂(20%甘露醇)治疗创伤脑水肿实验研究

用竖直落体致伤兔脑建立重型脑损伤模型,分别于伤后20分钟经颈动脉及周围静脉输注20％甘露醇,2小时后应用低温电子自旋共振(ESR)技术检测损伤脑区组织中脂质过氧化自由基(ROO·)含量,并同步观察脑组织含水量、病理学及超微结构改变,探讨不同输注途径的治疗效果。结果表明颈动脉输注甘露醇能更显著降低损伤脑自由基幅值(Ymax)及脑组织含水量,并能明显减轻神经细胞、胶质细胞及血管周围的水肿及继发性脑损害。

Effects of Water─soluble Components Isolated from Salviamilltiorrhiza on Oxygen Free Radical Generation and LipidPeroxidation

The effects of water─soluble components isolated from Salvia miltiorrhiza on oxygen free radical prodction and lipid peroxidation were estimated. Five components(10 μmol/L)were shown to inhibit superoxide anion generation by xanthine─xanthine oxidase system. It was also demonstrated that six components( 100 μmol/L) prevented H_2O_2─induced hemolysis and MDA fonnation in mouse erythrocytes.The effects of Sal A, Sal B, Sal C and Ros A were dose dependent. In Langendorff rat heart, pretreatment with Sal A 20μmol/L significantly prevented MDA production induced by 30 min reoxygenation after 45 min anoxia.The results indicated that there were also other potent antioxidant componentts in Salvia milliorrhiza besides Dphl and Pal. The protection of Sal A against myocardial anoxiareoxygenation inury may be mainly ascribed to its oxygen free radical scavenging activity.

Mechanisms of Inhibitory Effects of Breviscapine on Lipid Peroxidation in Rat Brain Mitochondria

The mechanisms by which breviscapine (Bre) inhibits the lipid preoxidation in rat brain mitochondria were investigated. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. The chelating activities of Bre for Fe 2+ were tested by differential spectrum. Superoxide anion (O 2)from xanthine xanthine oxidase (Xan XO) system and hydroxyl radical (·OH) from FeSO 4 H 2O 2 system were determined with spectrophotometry. It was found that Bre could effectively inhibit the lipid peroxidation of brain mitochondria induced by free radicals driven from Xan XO and FeSO 4 H 2O 2 system. The IC 50 of Bre were 93 01 μmol·L -1 for Xan XO system and 62 18 μmol·L -1 for FeSO 4 H 2O 2 system. Bre also scavenged O 2 and ·OH produced by Xan XO and FeSO 4 H 2O 2 systems. The IC 50 of Bre were 32 63 μmol·L -1 for O - 2 and 20 22 μmol·L -1 for ·OH. Furthermore, the chelating Fe 2+ activity of Bre was shown. It may be concluded that Bre inhibited lipid peroxidation at different stages of the reaction of oxygen free redial with the mitochondria membrane: (1) the formation of ·OH; (2) the initiation of the lipid peroxidation, by chelating Fe 2+ and scavenging O 2 as well as ·OH. The scavenging oxygen free radicals and chelating iron are the mechanisms of inhibitory effect of Bre on lipid peroxidation.

茶多酚:为健康加分

老年人常见慢性病主要有恶性肿瘤、心脑血管疾病和糖尿病三大类．这些疾病的发生和体内氧自由基泛滥有一定关系。因此，清除过量氧自由基，减少体内脂质过氧化物生成，对预防各种慢性病意义重大。茶萃茶多酚胶囊对各种氧自由基如超氧阴离子自由基、羟基自由基、脂质过氧化自由基等有清除作用，效果更好。因此，补充高效抗氧化物茶多酚，对预防上述三种慢’陛病非常有益。茶多酚至少对以下6种疾病防治有益。

降糖药达美康可降低心肌梗死的危险

丹麦一项病例对照研究，纳入6738例心肌梗死患者和67374例对照，观察新型磺脲类降糖药达美康（格列齐特）和格列美脲（亚莫利）与其他磺脲类如格列本脲（优降糖）、格列吡嗪（美吡达）、甲苯磺丁脲（D860）对心肌梗死病死率的影响。结果：心肌梗死30天病死率，达美康组（9．5％）显著低于服用其他磺脲类降糖药组（30％～34．3％）。此研究表明，达美康还可清除过氧化自由基和减少氧化应激反应对心血管的损害，增强一氧化氮对血管的扩张，从而对心血管起到一定的保护作用。

Antioxidative capacity and enzyme activity in Haematococcus pluvialis cells exposed to superoxide free radicals

The antioxidative capacity of astaxanthin and enzyme activity of reactive oxygen eliminating enzymes such as superoxide dismutase (SOD),peroxidase (POD),catalase (CAT) and ascorbate peroxidase (APX) were studied in three cell types of Haematococcus pluvialis exposed to high concentrations of a superoxide anion radical (O2ˉ).The results show that defensive enzymes and astaxanthin-related mechanisms were both active in H.pluvialis during exposure to reactive oxygen species (ROS) such as Oˉ2.Astaxanthin reacted with ROS much faster than did the protective enzymes,and had the strongest antioxidative capacity to protect against lipid peroxidation.The defensive mechanisms varied significantly between the three cell types and were related to the level of astaxanthin that had accumulated in those cells.Astaxanthin-enriched red cells had the strongest antioxidative capacity,followed by brown cells,and astaxanthin-deficient green cells.Although there was no significant increase in expression of protective enzymes,the malondialdehyde (MDA) content in red cells was sustained at a low level because of the antioxidative effect of astaxanthin,which quenched Oˉ2 before the protective enzymes could act.In green cells,astaxanthin is very low or absent;therefore,scavenging of ROS is inevitably reliant on antioxidative enzymes.Accordingly,in green cells,these enzymes play the leading role in scavenging ROS,and the expression of these enzymes is rapidly increased to reduce excessive ROS.However,because ROS were constantly increased in this study,the enhance enzyme activity in the green cells was not able to repair the ROS damage,leading to elevated MDA content.Of the four defensive enzymes measured in astaxanthin-deficient green cells,SOD eliminates Oˉ2,POD eliminates H2O2,which is a by-product of SOD activity,and APX and CAT are then initiated to scavenge excessive ROS.