Evaluation of malondialdehyde as an index of lead damage in rat brain homogenates
Evaluation of malondialdehyde as an index of lead damage in rat brain homogenates
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DOI：
10.1007/bf00141599
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发表时间：
1995-10
期刊：
影响因子：
3.5
通讯作者：
Shafiq-Ur-Rehman;Shaheen Rehman;O. Chandra;M. Abdulla
中科院分区：
文献类型：
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作者：
Shafiq-Ur-Rehman;Shaheen Rehman;O. Chandra;M. Abdulla
作为铅中毒的后遗症，研究了脑体外匀浆中的脂质过氧化。测定铅（50μg）单独或与抗坏血酸（100μg）、α -酚（100μg）、对苯二酚（100μg）联合处理大鼠脑匀浆（1 ml, 5% w/v）中丙二醛（MDA）的含量。铅诱发丙二醛水平呈剂量相关性。铅的毒性随着抗坏血酸对大脑的作用而进一步增强。然而，抗氧化药物α -酚和对苯二酚降低了铅对大脑的毒性作用。这些结果清楚地表明，脂质过氧化的增强可能为铅诱导的神经毒性提供了基础。
Lipid peroxidationin vitrohomogenates of brain was examined as sequela of lead toxicity. The levels of malondialdehyde (MDA) in homogenates of rat brain (1 ml, 5% w/v) treated with lead (50μg) alone or in combination with ascorbic acid (100μg), alphatocopherol (100μg) or hydroquinone (100μg) were evaluated. The levels of MDA were consistently evoked by lead in a dose-related manner. The toxicity of lead was further advanced by the action of the pro-oxidant drug ascorbic acid on the brain. However, the anti-oxidant drugs alphatocopherol and hydroquinone decreased the toxic effect of lead on the brain. These results clearly show that the enhanced lipid peroxidation may provide a basis of lead-induced neurotoxicity.