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首页> 外文期刊>Life sciences >Lipid peroxidation induced by phenylbutazone radicals.
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Lipid peroxidation induced by phenylbutazone radicals.

机译：苯基丁a自由基引起的脂质过氧化。

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摘要

Lipid peroxidation was investigated to evaluate the deleterious effect on tissues by phenylbutazone (PB). PB induced lipid peroxidation of microsomes in the presence of horseradish peroxidase and hydrogen peroxide (HRP-H2O2). The lipid peroxidation was completely inhibited by catalase but not by superoxide dismutase. Mannitol and dimethylsulfoxide had no effect. These results indicated no paticipation of superoxide and hydroxyl radical in the lipid peroxidation. Reduced glutathione (GSH) efficiently inhibited the lipid peroxidation. PB radicals emitted electron spin resonance (ESR) signals during the reaction of PB with HRP-H2O2. Microsomes and arachidonic acid strongly diminished the ESR signals, indicating that PB radicals directly react with unsaturated lipids of microsomes to cause thiobarbituric acid reactive substances. GSH sharply diminished the ESR signals of PB radicals, suggesting that GSH scavenges PB radicals to inhibit lipid peroxidation. Also, 2-methyl-2-nitrosopropan strongly inhibited lipid peroxidation. R-Phycoerythrin, a peroxyl radical detector substance, was decomposed by PB with HRP-H2O2. These results suggest that lipid peroxidation of microsomes is induced by PB radicals or peroxyl radicals, or both.
机译：研究了脂质过氧化作用，以评估苯基丁a（PB）对组织的有害作用。 PB在辣根过氧化物酶和过氧化氢（HRP-H2O2）存在下诱导微粒体脂质过氧化。过氧化氢酶完全抑制了脂质的过氧化，但超氧化物歧化酶则没有。甘露醇和二甲基亚砜无作用。这些结果表明脂质过氧化中没有超氧化物和羟基自由基的参与。还原型谷胱甘肽（GSH）有效抑制脂质过氧化。 PB自由基在PB与HRP-H2O2反应期间发出电子自旋共振（ESR）信号。微粒体和花生四烯酸极大地减弱了ESR信号，表明PB自由基直接与微粒体的不饱和脂质反应，从而导致硫代巴比妥酸反应性物质。 GSH大大降低了PB自由基的ESR信号，表明GSH清除了PB自由基以抑制脂质过氧化。同样，2-甲基-2-亚硝基丙烷也强烈抑制脂质过氧化。过氧自由基检测剂R-藻红蛋白被PB用HRP-H2O2分解。这些结果表明微粒体的脂质过氧化被PB自由基或过氧自由基或两者诱导。

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