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二氯甲烷的肝毒性。

Hepatotoxicity of dichloromethane.

作者信息

Mizutani K, Shinomiya K, Shinomiya T

机构信息

1st Department of Surgery, Ehime University, Japan.

出版信息

Forensic Sci Int. 1988 Jul-Aug;38(1-2):113-28. doi: 10.1016/0379-0738(88)90015-1.

Abstract

We studied hepatotoxicity of dichloromethane using primary cultures of parenchymal cells (hepatocyte) from adult rat livers. The production of carbon monoxide from dichloromethane increased with time, the increased cell number, and the concentration of dichloromethane. However, the carbon monoxide production per hepatocyte decreased with increasing cell density. When dichloromethane was in a high concentration, the metabolism of dichloromethane to carbon monoxide was extensively depressed, total glutamic-oxaloacetic transaminase (GOT) and mitochondrial GOT (m-GOT) levels in the cultured medium were extensively elevated, and the cultured hepatocytes were destroyed by dichloromethane. A case of accidental exposure to dichloromethane which occurred in Japan was also considered, and it is suspected that the inhalation of dichloromethane vapors in a high concentration for many hours may cause hepatotoxicity.

摘要

我们使用成年大鼠肝脏实质细胞(肝细胞)的原代培养物研究了二氯甲烷的肝毒性。二氯甲烷产生一氧化碳的量随时间、细胞数量增加以及二氯甲烷浓度的升高而增加。然而,每个肝细胞产生一氧化碳的量随细胞密度增加而减少。当二氯甲烷处于高浓度时,二氯甲烷向一氧化碳的代谢被广泛抑制,培养基中总谷氨酸草酰乙酸转氨酶(GOT)和线粒体GOT(m-GOT)水平大幅升高,培养的肝细胞被二氯甲烷破坏。还考虑了在日本发生的一起二氯甲烷意外暴露事件,怀疑长时间高浓度吸入二氯甲烷蒸气可能会导致肝毒性。

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