Rehman S, Chandra O, Abdulla M
Department of Pharmacology, J. N. Medical College, Muslim University, Aligarh, India.
Biometals. 1995 Oct;8(4):275-9. doi: 10.1007/BF00141599.
Lipid peroxidation in vitro homogenates 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 (50 micrograms) alone or in combination with ascorbic acid (100 micrograms), alphatocopherol (100 micrograms) or hydroquinone (100 micrograms) 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.
研究了脑体外匀浆中的脂质过氧化作为铅毒性后遗症的情况。评估了单独用铅（50微克）或与抗坏血酸（100微克）、α-生育酚（100微克）或对苯二酚（100微克）联合处理的大鼠脑匀浆（1毫升，5%重量/体积）中丙二醛（MDA）的水平。铅以剂量相关的方式持续诱发MDA水平升高。促氧化药物抗坏血酸对脑的作用进一步加重了铅的毒性。然而，抗氧化药物α-生育酚和对苯二酚降低了铅对脑的毒性作用。这些结果清楚地表明，脂质过氧化增强可能是铅诱导神经毒性的基础。
