有机磷酸酯抑制牛肾上腺嗜铬细胞中儿茶酚胺的分泌和钙内流。

Organophosphates inhibit catecholamine secretion and calcium influx in bovine adrenal chromaffin cells.

作者信息

Liu P S, Kao L S, Lin M K

机构信息

Department of Microbiology, Soochow University, Shihlin, Taipei, Taiwan, ROC.

出版信息

Toxicology. 1994 May 31;90(1-2):81-91. doi: 10.1016/0300-483x(94)90207-0.

DOI:10.1016/0300-483x(94)90207-0

PMID:8023345

Abstract

The lethality of organophosphorous compounds has been attributed to their inhibitory effect on acetylcholinesterase (AChE) in the nervous system. However, subacute exposure of humans to organophosphates induces cognitive and emotional defects which might not solely be attributable to AChE inhibition. Therefore we investigated the toxic effects of methyl parathion and malathion on bovine adrenal chromaffin cells. Catecholamine secretion and 45Ca2+ uptake evoked by either a nicotinic agonist (DMPP) or high [K+] were inhibited by methyl parathion and malathion. The [Ca2+]i rise induced by DMPP was inhibited by both compounds. We conclude that in addition to AChE, voltage-gated Ca2+ channels and nicotinic receptors are possible sites of action of organophosphates in mammalian systems.

摘要

有机磷化合物的致死性归因于它们对神经系统中乙酰胆碱酯酶（AChE）的抑制作用。然而，人类亚急性接触有机磷会诱发认知和情绪缺陷，这可能不完全归因于AChE抑制。因此，我们研究了甲基对硫磷和马拉硫磷对牛肾上腺嗜铬细胞的毒性作用。甲基对硫磷和马拉硫磷抑制了烟碱激动剂（DMPP）或高[K+]诱发的儿茶酚胺分泌和45Ca2+摄取。两种化合物均抑制了DMPP诱导的[Ca2+]i升高。我们得出结论，除AChE外，电压门控Ca2+通道和烟碱受体可能是有机磷在哺乳动物系统中的作用位点。