Flora G J, Seth P K
Division of Developmental Toxicity, Industrial Toxicology Research Centre, M.G. Marg, Lucknow, India.
Cytobios. 2000;103(403):103-9.
The effect of lead exposure on intracellular calcium levels, membrane fluidity, lipid peroxidation, acetylcholinesterase and monoamine oxidase activity and its accumulation in different regions of the brain were studied to understand the molecular mechanism of lead induced neurotoxicity. Lead treatment (20 mg/kg lead nitrate, intraperitoneally, once daily for 15 days) resulted in a significant accumulation of lead in all brain regions with the maximum being in the hippocampus. Levels of glutathione, lipid peroxidation, intracellular calcium and membrane fluidity, as well as the activity of the membrane bound enzymes, acetylcholinesterase and monoamine oxidase, increased to a significant level in certain areas of the rat brain. The results suggest that lead exerts neurotoxic effects by altering certain membrane bound enzymes and may cause oxidative stress.
研究了铅暴露对细胞内钙水平、膜流动性、脂质过氧化、乙酰胆碱酯酶和单胺氧化酶活性的影响及其在大脑不同区域的蓄积情况,以了解铅诱导神经毒性的分子机制。铅处理(腹腔注射20mg/kg硝酸铅,每天一次,持续15天)导致所有脑区铅显著蓄积,其中海马区蓄积量最大。大鼠脑某些区域的谷胱甘肽水平、脂质过氧化、细胞内钙和膜流动性以及膜结合酶乙酰胆碱酯酶和单胺氧化酶的活性均显著升高。结果表明,铅通过改变某些膜结合酶发挥神经毒性作用,并可能导致氧化应激。