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甲基汞中毒主要表现为精神和行为上的障碍,其机理尚不清楚。尤其是未产生病理损伤剂量的低浓度甲基汞,对中枢神经系统的作用所知更少。Taylor曾报道亚临床剂量水平的甲基汞,使幼鼠脑中生物胺的含量减少,并降低5-羟色胺更新率。同时发现色氨酸羟化酶的活性降低。据报道甲基汞能干扰脑的介质传递对中枢神经系统产生强力的毒性作用。不少学者认为甲基汞引起介质传递的障碍可能与神经末梢介质的摄取、释放和贮存过程障碍有关。因此,作者选用大鼠脑突触小体,研究了甲基汞对中枢神经系统中单胺摄取和释放的作用。
Methylmercury poisoning is mainly manifested as mental and behavioral disorders, and the mechanism is not clear. In particular, methylmercury, a low concentration of methyl mercury that does not produce a dose of pathological damage, is less known for its effects on the central nervous system. Taylor has reported subclinical methylmercury levels that reduce the biogenic amine content in the brains of young rats and decrease the 5-HT seroconversion rate. At the same time tryptophan hydroxylase activity was found to decrease. It has been reported that methylmercury interferes with the potent toxic effects of the brain’s transmission of the medium on the central nervous system. Many scholars believe that methylmercury-induced barriers to the transmission of media may be associated with nerve endings media uptake, release and storage process barriers. Therefore, the authors selected rat brain synaptosomes to study the effect of methylmercury on monoamine uptake and release in the central nervous system.