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母体镉暴露或给胎鼠注射镉对胎鼠肝脏金属硫蛋白浓度的影响。

The influence of maternal cadmium exposure or fetal cadmium injection on hepatic metallothionein concentrations in the fetal rat.

作者信息

Sasser L B, Kelman B J, Levin A A, Miller R K

出版信息

Toxicol Appl Pharmacol. 1985 Sep 15;80(2):299-307. doi: 10.1016/0041-008x(85)90087-0.

Abstract

The ability of Cd to induce the synthesis of fetal hepatic metallothionein (MT) was investigated in rat fetuses exposed to Cd throughout gestation via the mother's drinking water or injected directly with Cd through the uterine wall on Day 18 of gestation. On Day 21 all dams were killed and fetal and maternal tissues were removed. Tissue MT, Zn, Cu, and Cd concentrations were measured. Fetal hepatic Cd concentration was increased only at the high maternal Cd exposure, whereas Zn concentration was significantly reduced by Cd exposure. Both fetal liver and kidney MT were reduced following maternal Cd exposure. Unlike maternal hepatic MT, fetal hepatic MT was not increased after maternal Cd exposure nor did the direct injection of Cd into the 18 days of gestation fetus induce fetal MT synthesis. These data suggest that fetal rat liver is incapable of synthesizing MT in response to Cd, possibly because Cd is not transported to the site of MT synthesis in the fetal system. Furthermore, neither the route of exposure, the duration of prenatal Cd exposure, nor the stage of gestation appear to account for the differences observed between fetal and adult hepatic MT induction by Cd.

摘要

通过母体饮用水在整个孕期使大鼠胎儿暴露于镉,或在妊娠第18天经子宫壁直接给大鼠胎儿注射镉,以此研究镉诱导胎儿肝脏金属硫蛋白(MT)合成的能力。在第21天,处死所有母鼠并取出胎儿和母体组织。测量组织中的MT、锌、铜和镉浓度。仅在母体高镉暴露时,胎儿肝脏镉浓度升高,而镉暴露使锌浓度显著降低。母体镉暴露后,胎儿肝脏和肾脏的MT均减少。与母体肝脏MT不同,母体镉暴露后胎儿肝脏MT未增加,向妊娠18天的胎儿直接注射镉也未诱导胎儿MT合成。这些数据表明,胎鼠肝脏无法响应镉合成MT,这可能是因为镉未转运至胎儿系统中MT的合成部位。此外,暴露途径、产前镉暴露持续时间或妊娠阶段似乎均无法解释镉诱导胎儿和成年肝脏MT产生差异的原因。

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