Nehru B, Kanwar S S
Department of Biophysics, Panjab University, Chandigarh, India.
Biol Trace Elem Res. 2004 Dec;101(3):257-64. doi: 10.1385/BTER:101:3:257.
Lead (Pb) is known to disrupt the pro-oxidant/antioxidant balance of tissues, which leads to biochemical and physiological dysfunction. Oxidative stress is considered a possible molecular mechanism involved in Pb neurotoxicity. Considering the vulnerability of the brain to oxidative stress under Pb neurotoxicity, this study investigated the effects of exposure of the thiol antioxidant N-acetylcysteine (NAC) on lead-induced oxidative damage and lipid peroxidation in brain regions of the rat. Wister strain rats were exposed to lead in the form of lead acetate (20 mg/kg body wt/d) for a period of 2 wk and the effects of NAC on lead-induced neurotoxicity in rat brain regions were assessed by postadministration of NAC (160 mg/kg body wt/d) for a period of 3 wk. The lipid peroxidation byproduct, malondialdehyde (MDA) increased following lead exposure in both of the regions, and the antioxidant capacities of the cell in terms of the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) was diminished. Following NAC treatment, lead-induced lipid peroxidation decreased and antioxidant enzyme activities improved, with CAT showing enhancement in the cerebral region only and SOD showing enhancements in the cerebellar region. Our result suggests that thiol-antioxidant supplementation following Pb exposure might enhance the reductive status of brain regions by arresting the lipid peroxidative damage in brain regions.
已知铅（Pb）会破坏组织的促氧化剂/抗氧化剂平衡，从而导致生化和生理功能障碍。氧化应激被认为是铅神经毒性可能涉及的分子机制。考虑到在铅神经毒性作用下大脑对氧化应激的易感性，本研究调查了硫醇抗氧化剂N-乙酰半胱氨酸（NAC）对大鼠脑区铅诱导的氧化损伤和脂质过氧化的影响。将Wister品系大鼠以醋酸铅（20毫克/千克体重/天）的形式暴露于铅中2周，通过在给予NAC（160毫克/千克体重/天）3周后评估NAC对大鼠脑区铅诱导的神经毒性的影响。在两个脑区中，铅暴露后脂质过氧化副产物丙二醛（MDA）增加，并且细胞抗氧化酶超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性方面的抗氧化能力降低。NAC处理后，铅诱导的脂质过氧化减少，抗氧化酶活性提高，CAT仅在大脑区域显示增强，而SOD在小脑区域显示增强。我们的结果表明，铅暴露后补充硫醇抗氧化剂可能通过阻止脑区脂质过氧化损伤来增强脑区的还原状态。
