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甲基汞诱导小鼠急性肾功能障碍中的性别差异。

Sex difference in acute renal dysfunction induced by methylmercury in mice.

作者信息

Yasutake A, Hirayama K, Inouye M

机构信息

National Institute for Minamata Disease, Kumamoto, Japan.

出版信息

Ren Fail. 1990;12(4):233-40. doi: 10.3109/08860229009060730.

Abstract

To investigate the sex-related difference of susceptibility of renal function to methylmercury (MeHg) toxicity, various doses of MeHg chloride (MMC, 20-200 mumol/kg) were orally administered to C57BL/6N mice of both sexes. On days 1, 3, 5, and 7 after MMC administration, the extent of damage to renal function and the renal Hg levels were examined. After dosing, female mice survived much longer than males. With the increase in the dose level to 200 mumol/kg, the changes of the renal Hg levels 24 h after administration showed biphasic features with a plateau of around 85 micrograms/g. The renal Hg in male mice increased more rapidly to the plateau than in females. The doses by which the renal Hg level reached the plateau were 80 and 120 mumol/kg for males and females, respectively. The time-dependent decrease of the renal Hg became much slower with dose levels exceeding 80 and 160 mumol/kg for males and females, respectively. Inhibition of phenolsulfonphthalein excretion and increase of plasma creatinine after the MMC administration were more marked in males than in females. Inorganic Hg levels in the kidney of MeHg-intoxicated mice were much lower than that of HgCl2-intoxicated mice, indicating that the involvement of inorganic Hg, a product of biotransformation of MeHg, in the renal failure caused by MMC treatment would be negligible. Although pathological changes in the renal proximal tubules of HgCl2-intoxicated mice were marked, those of the MeHg-intoxicated group were slight.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

为研究肾功能对甲基汞(MeHg)毒性易感性的性别差异,对两性C57BL/6N小鼠口服给予不同剂量的氯化甲基汞(MMC,20 - 200 μmol/kg)。在给予MMC后的第1、3、5和7天,检测肾功能损害程度和肾脏汞含量。给药后,雌性小鼠存活时间比雄性长得多。随着剂量水平增加到200 μmol/kg,给药后24小时肾脏汞含量变化呈现双相特征,平台期约为85微克/克。雄性小鼠肾脏汞含量比雌性更快达到平台期。雄性和雌性小鼠肾脏汞含量达到平台期的剂量分别为80和120 μmol/kg。当剂量水平分别超过雄性80 μmol/kg和雌性160 μmol/kg时,肾脏汞含量随时间的下降变得慢得多。MMC给药后,雄性小鼠酚红排泄的抑制和血浆肌酐的增加比雌性更明显。甲基汞中毒小鼠肾脏中的无机汞含量远低于氯化汞中毒小鼠,这表明甲基汞生物转化产物无机汞在MMC治疗引起的肾衰竭中的作用可忽略不计。虽然氯化汞中毒小鼠肾近端小管的病理变化明显,但甲基汞中毒组的变化轻微。(摘要截短于250字)

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