35种鲜花的抗氧化活性

采用了Fe^2 诱发的脂蛋白PUFA过氧化、H2O2诱导的RBC溶血和紫外线（UV）诱发的RBC溶血等3个体外抗氧化实验体系,对映山红（Rhododendron simsii Planch.)等35种鲜花的抗氧化活性进行了测定和比较。结果表明,在所测定的35种鲜花中,4种杜鹃属（Rhododendron L.)植物的花勒抗氧化活性最强。一定浓度白杜鹃[R.mucronatum (Blume)G.Don]花蕾提取液的抗Fe^2 诱发的脂蛋白PUFA过氧化活性明显高于维生素C。     

甲状腺病理条件下兔肝中的Fe~(2 )与脂质过氧化

Ｆｅ２＋在缺血缺氧／再复氧所致脂质过氧化中的作用已被许多研究证实。为了探讨在伴随有脂质过氧化激活的其它病理过程中Ｆｅ２＋的作用,本实验以家兔为模型,采用化学发光（ＣＬ）和电子自旋共振（ＥＳＲ）技术分别对甲状腺病理条件下肝组织中脂质过氧化水平和肝细胞中...     

Fe（Ⅱ）离子所引发的羟自由基对人红细胞膜的作用

Ｆｅ（Ⅱ）离子所引发的羟自由基对人红细胞膜的作用薄云红,徐轶,王夔（北京医科大学药学院,北京１０００８３））在人体内由铁催化产生的·ＯＨ会引发脂质过氧化链式反应,而且在维生素Ｃ（Ｖｃ）存在下其过氧化程度加剧,导致红细胞膜构象改变［１］。血红素是一种富...     

渗透胁迫下稻苗中铁催化的膜脂过氧化作用

在－０．７ＭＰａ渗透胁迫下,水稻幼苗体内和Ｈ２Ｏ２大量产生,Ｆｅ２＋积累,膜脂过氧化作用加剧。水稻幼苗体内Ｆｅ２＋含量与膜脂过氧化产物ＭＤＡ含量呈极显著的正相关。外源Ｆｅ２＋、Ｆｅ３＋、Ｈ２Ｏ２、Ｆｅ２＋＋Ｈ２Ｏ２、ＤＤＴＣ均能刺激膜脂过氧化作用,而铁离子的螯合剂ＤＴＰＡ则有缓解作用。ＯＨ的清除剂苯甲酸钠和甘露醇能明显地抑制渗透胁迫下Ｆｅ２＋催化的膜脂过氧化作用。这都表明渗透胁迫下水稻幼苗体内铁诱导的膜脂过氧化作用主要是由于其催化Ｆｅｎｔｏｎ型Ｈａｂｅｒ－Ｗｅｉｓｓ反应形成ＯＨ所致。     

甘青铁线莲花水提取物的抗氧化活性研究

本文采用邻二氮菲-Fe2 氧化法,邻苯三酚自氧化法以及卵黄脂蛋白不饱和脂肪酸(PUFA)过氧化体系,对甘青铁线莲花水提取物清除超氧阴离子自由基(O-·2 )和羟自由基(·OH )以及抑制卵黄脂蛋白脂质过氧化(LPO)作用的效果进行了测定.结果表明:甘青铁线莲花水提取物有清除O-2、OH的能力,同时能抑制卵黄脂蛋白脂质过氧化(LPO)作用,在相同干物质浓度下(黄酮含量为2.20 μg),抑制卵黄脂蛋白脂质过氧化(LPO)作用最强、O-2次之、OH最弱,这说明甘青铁线莲花水提取物有抗氧化作用,且水提物抗氧化活性在一定浓度范围内与其黄酮类化合物含量呈正相关.     

黄皮种子脱水敏感性与脂质过氧化作用

黄皮种子自然脱水时,种子的发芽率和发芽指数迅速下降;种子浸泡液的电导率和可溶性物质的量大大增加;线粒体膜和质膜ATPase的活性下降;种子中SOD活性先上升,然后下降;脂质过氧化产物MDA和脂质氢过氧化物的量大大增加。DDC、MDA和Fe2 促进脂质过氧化作用,降低种子生活力;ASA和甘露醇对脂质过氧化有抑制作用,提高种子生活力。     

内源性Fe^2＋在鼠肝缺血缺氧再给氧后脂质过氧化中的作用

内源性Ｆｅ２＋在鼠肝缺血缺氧再给氧后脂质过氧化中的作用刘振宅（天津医科大学生物医学工程系,天津３０００７０）许多病理过程都伴有器官和组织的局部缺血,缺血缺氧后再给氧时脂质过氧化作用急剧增强,导致组织不可逆损伤和坏死。本文建立了鼠肝缺血缺氧再给氧模型,...     

麦草粉的抗氧化作用研究

测定了大麦和黑麦草嫩叶汁粉的小鼠肝脂质过氧化作用和抗油脂过氧化作用。结果表明,麦草汁粉具有显著的抗小鼠肝脂质过氧化作用,抑制率分别达38．23％（大麦嫩叶汁粉）和69．16％（黑麦草嫩叶汁粉）;对油脂的过氧化也具有一定的抑制作用。麦草汁粉的抗氧化作用主要与其所含酚性物质有关。     

集落刺激因子与动脉粥样硬化

集落刺激因子（ＣＳＦｓ）可通过激活ＬＤＬ受体依赖性和非依赖性途径，使含ＡＰＯＢ－１００的脂蛋白水平降低。另一方面，动脉壁内ＣＳＦｓ则吸引循环单核细胞而聚集、衍化为巨噬细胞，并增强其摄取脂蛋白和酯化胆固醇的能力。提示ＣＳＦｓ对动脉粥样硬化可能具有抑制和促进双重作用。对ＷＨＨＬ兔的整体实验显示，Ｍ－ＣＳＦ能减缓其自发性动脉粥样硬化的进程。对ＣＳＦｓ的进一步研究可能有助于加深对动脉粥样硬化发病机理的认识，进而开辟防治新途径。     

籽鹅卵泡颗粒细胞烯醇化酶过表达模型的建立及其对孕酮分泌的影响

目的：建立廿烯醇化酶（EN01）腺病毒过表达载体转染原代培养籽鹅卵泡颗粒细胞模型,探讨EN01过表达对颗粒细胞孕酮分泌的影响。方法：采用EN01腺病毒过表达载体以梯度感染复数值（MOI）100、250、350、400pfu／cell转染原代培养籽鹅卵泡颗粒细胞,于转染后2,4h、48h,荧光倒置显微镜下观察绿色荧光蛋白（GFP）表达。双抗体一步夹心法酶联免疫吸附试验（EusA）研究EN01过表达对颗粒细胞孕酮分泌的影响。结果：最佳转染条件是,当MOI为350pfu／cell,转染48h后,转染率达100％;通过荧光定量PCR与Westernblot法,检测到EN01mRNA与蛋白均过表达（P〈0．01）;与培养液组和腺病毒空载体组相比较,EN01过表达使颗粒细胞孕酮分泌量极显著增加（P〈0．01）。结论：EN01过表达会使体外原代培养的籽鹅卵泡颗粒细胞孕酮分泌量增加。     

An investigation into the role of hydroxyl radical in xanthine oxidase-dependent lipid peroxidation

A model lipid peroxidation system dependent upon the hydroxyl radical, generated by Fenton's reagent, was compared to another model system dependent upon the enzymatic generation of superoxide by xanthine oxidase. Peroxidation was studied in detergent-dispersed linoleic acid and in phospholipid liposomes. Hydroxyl radical generation by Fenton's reagent (FeCl₂ + H₂O₂) in the presence of phospholipid liposomes resulted in lipid peroxidation as evidenced by malondialdehyde and lipid hydroperoxide formation. Catalase, mannitol, and Tris-Cl were capable of inhibiting activity. The addition of EDTA resulted in complete inhibition of activity when the concentration of EDTA exceeded the concentration of Fe²⁺. The addition of ADP resulted in slight inhibition of activity, however, the activity was less sensitive to inhibition by mannitol. At an ADP to Fe²⁺ molar ratio of 10 to 1, 10 mm mannitol caused 25% inhibition of activity. Lipid peroxidation dependent on the enzymatic generation of superoxide by xanthine oxidase was studied in liposomes and in detergent-dispersed linoleate. No activity was observed in the absence of added iron. Activity and the apparent mechanism of initiation was dependent upon iron chelation. The addition of EDTA-chelated iron to the detergent-dispersed linoleate system resulted in lipid peroxidation as evidenced by diene conjugation. This activity was inhibited by catalase and hydroxyl radical trapping agents. In contrast, no activity was observed with phospholipid liposomes when iron was chelated with EDTA. The peroxidation of liposomes required ADP-chelated iron and activity was stimulated upon the addition of EDTA-chelated iron. The peroxidation of detergent-dispersed linoleate was also enhanced by ADP-chelated iron. Again, this peroxidation in the presence of ADP-chelated iron was not sensitive to catalase or hydroxyl radical trapping agents. It is proposed that initiation of superoxide-dependent lipid peroxidation in the presence of EDTA-chelated iron occurs via the hydroxyl radical. However, in the presence of ADP-chelated iron, the participation of the free hydroxyl radical is minimal.     

Activity of the glutathione antioxidant system and cytochrome P-450 in rat liver under induction and inhibition of xanthine oxidase

The effects of specific xanthine oxidase induction and inhibition on glutathione antioxidant system activity, lipid peroxidation, cytochrome P-450 quantity and corticosteroids concentration in the rat liver were studied. It was dependence established that there was a straight between xanthine oxidase activity and the activity of glutathione antioxidant system, lipid peroxidation and the ascorbic acid formation. The reciprocal dependence was established between xanthine oxidase activity and the concentrations of cytochrome P-450 and corticosteroids.     

Phylo- and ontogenic characteristics of lipid peroxidation in the retina of vertebrates

Phylo- and ontogenetic aspects of lipid peroxidation and antioxidative enzyme system in the retina of vertebrates were studied. It was established that both the intensity of lipid peroxidation and the activity of glutathione peroxidase in the retina of different vertebrate animals (carp, frog, tortoise, pigeon, rabbit) considerably diminished with evolution. The differences in the intensity of lipid peroxidation and the activity of glutathione peroxidase between dark- and light-adapted retinas also decreased depending on the level of the development. The activity of glutathione peroxidase in the retina of chick embryos was found only at the end of the incubation period.     

Lipid peroxidation and myocardial contractile function in the post-ischemic period depending on the level of hypothermic protection of the heart]

The experiments on rats isolated hearts showed lipid peroxidation state to depend on myocardial cooling level in ischemic period. Cooling to 8-12 degrees C does not induce significant impairment in the system of lipid peroxidation/antioxidant activity, thus preventing the development of reperfusion impairment in cardiac activity restoration. Temperature decrease to 4-6 degrees C during the ischemic period results in lipid peroxidation, antioxidant cell system exhaustion and impairment of contractive myocardial function in reperfusion.     

Changes in the activity of antioxidant enzymes and level of lipid peroxidation in the embryo brain tissue during prenatal action of ethanol]

Catalase, superoxide dismutase (SOD) activity and level of lipid peroxidation in embryo brain of 13-17-th day were evaluated during ethanol consumption by pregnant rats. The level of lipid peroxidation was more higher in alcohol groups, than in control groups. At the same time the reduced glutathione content was decreased by 13% in the brain of 15-th day embryos under the same conditions. One can draw a conclusion that the elevated level of lipid peroxidation may be a consequence of activated free radical mechanisms or consequence of reduced activity of a non-enzymatic antioxidant system.     

Inhibition of the antioxidative activity of plasma by sodium azide

Powerful antioxidant activity of human plasma was demonstrated by measuring the thiobarbituric acid reaction and Fe+2-induced chemiluminescence. Inhibition of lipid peroxidation was shown both for plasma lipids and for the suspension of egg lipoproteins, which was taken as a model system. The inhibitory effect of plasma peroxidation was removed by azide Na taken in the concentration of 0.5 mg/ml, but caeroplasmin activity in the plasma was completely suppressed at NaN3 concentration equal to 0.1 mg/ml. A low correlation (r = 0.75) between caeruloplasmin activity in the blood plasma and extent of chemiluminescence activation obtained in the presence of NaN3 was found. The presented data led to an assumption that only a part of lipid peroxidation inhibitors in the plasma can be attributed with caeruloplasmin.     

Partial characterization of the inhibitory effect of lipid peroxidation on the ouabain-insensitive Na-ATPase of rat kidney cortex plasma membranes

The present work evaluates the effect of lipid peroxidation on the ouabain-insensitive Na-ATPase of basolateral plasma membranes from rat kidney proximal tubular cells as an indirect way to study the lipid dependence of this enzyme. An inverse relationship between lipid peroxidation and Na-ATPase activity was found. This effect was due neither to a change in the optimalK _m of the system for Na⁺ nor for the substrate Mg : ATP, nor the optimal pH value of the medium. The optimal temperature value, however, was shifted toward a higher value. There was also an increase of the apparent energy of activation in the region of temperatures above the transition point (20°C) with increase in lipid peroxidation. Peroxidized membranes incubated with phosphatidylcholine from soybean restored their Na-ATPase activity. On the other hand, the Na-ATPase activity was sensitive to oleoly lysophosphatidylcholine. These results suggest that lipid peroxidation might be affecting the Na-ATPase activity through either an increase of peroxidized phospholipids, which might change the membrane fluidity of the lipid microenvironment of the ATPase molecules, or through a direct effect of lysophospholipids released during the lipid peroxidation.     

Inhibitory Effects of Ebselen on Lipid Peroxidation in Rat Liver Microsomes

The effects of ebselen(2-pheny1-1,2-benzoisoselenazol-3(2H)-one), a synthetic seleno-organic compound with glutathione peroxidase-like activity were investigated on lipid peroxidation in rat liver microsomes. Ebselen inhibited malondialdehyde production coupled to the lipid peroxidation stimulated by either ADP-iron-ascorbate or CC1₄. The inhibitory activity of ebselen on each system was strongly increased by a 5-min preincubation with liver microsomes; the IC₅₀ values against ADP-Fe-ascorbate-stimulated and CC1₄-stimulated lipid peroxidation were 1.6/jM and 70 μM respectively. Ebselen also inhibited the endogenous lipid peroxidation with a NADPH-generating system, but it slightly stimulated the endogenous activity of ADP-Fe-ascorbate-stimulated lipid peroxidation (without a NADPH-generating system). Furthermore, ebselen inhibited oxygen uptake coupled to the lipid peroxidation by ADP-Fe-ascorbate and NADPH-ADP-iron; the IC₅₀ values were 2.5μM AND 20.3 μM respectively. Ebselen also prolonged the lag-time of onset of ADP-Fe-ascorbate-stimulated lipid peroxidation significantly, but not that observed with NADPH-ADP-Fe-stimulated lipid peroxidation.     

Importance of two iron-reducing systems in lipid peroxidation of rat brain: implications for oxygen toxicity in the central nervous system

The mechanism of lipid peroxidation in the central nervous system has been studied using oxygen-flushed rat brain homogenates at pH 7.4. Brain lipid peroxidation was monitored by chemiluminescence and by determination of thiobarbituric acid-reactive substances. Less involvement of O2-., H2O2 and probably .OH in the initiation of lipid peroxidation was indicated. Deferroxamine was an extremely potent inhibitor of lipid peroxidation, suggesting that lipid peroxidation was catalyzed by endogenous iron. Brain tissues were shown to contain at least two iron-reducing systems for promotion of lipid peroxidation. One was ascorbate-dependent and the other NADPH-dependent. The former was much more potent than the latter with respect to iron-reducing activity.     

Development of the cytosolic defence system against microsomal lipid peroxidation in rat liver

Ascorbate-induced lipid peroxidation in rat liver microsomes reaches the adult level in 2-3 days. NADPH-induced peroxidation develops more gradually, in parallel with the activity of NADPH-cytochrome P-450 reductase, attaining adult levels by 10-12 days. The glutathione-dependent cytosolic enzyme activity which inhibits peroxidation is inhibited by bromosulphophthalein. The development of this system lags behind the development of microsomal lipid peroxidation between the ages of 2 and 20 days, allowing peroxidation to proceed.