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乙醇可抑制摄入镉的怀孕大鼠后代大脑中的镉蓄积。

Ethanol inhibits cadmium accumulation in brains of offspring of pregnant rats that consume cadmium.

作者信息

Brus R, Kostrzewa R M, Felińska W, Plech A, Szkilnik R, Frydrych J

机构信息

Department of Pharmacology, Silesian Academy of Medicine, Zabrze, Poland.

出版信息

Toxicol Lett. 1995 Feb;76(1):57-62. doi: 10.1016/0378-4274(94)03198-3.

Abstract

The present study was designed to test the effect of ethanol on cadmium accumulation in tissues of pregnant rats and their offspring. Starting 10 days before mating and continuing until parturition, ethanol (10% v/v) was present in the drinking water of half the rats. Cadmium chloride (CdCl2; 50 ppm) was present in the water of half the rats (+/- ethanol) from the fist day after mating until parturition. On the day of parturition cadmium accumulated to a moderate level in bone (7.3 micrograms/g tissue, wet weight; this and other values, P < 0.05 vs. control), liver (12.9 micrograms/g) and kidney (13.0 micrograms/g) of dams, while the brain had only a low level of cadmium (0.45 microgram/g). In offspring at 6 weeks cadmium accumulated in high amounts in the brain (34.0 micrograms/g), bone (15.9 micrograms), kidney (78.2 micrograms/g) and particularly the liver (227.3 micrograms/g). Ethanol, given simultaneously with cadmium, inhibited cadmium accumulation in brain (1.8 micrograms/g), bone (3.28 micrograms/g) and kidney (61.3 micrograms/g), but enhanced cadmium accumulation in liver (408.7 micrograms/g). At 12 weeks there were only residual levels of cadmium in all tissues of offspring. These findings demonstrate an interaction between 2 known teratogenic agents, with ethanol conferring protection of the brain from cadmium accumulation. The nature of this interaction is not known, but is likely to be related to ethanol induction of metallothionein in the liver and placenta.

摘要

本研究旨在测试乙醇对孕鼠及其后代组织中镉蓄积的影响。从交配前10天开始,一直持续到分娩,一半的大鼠饮用水中含有乙醇(10% v/v)。从交配后第一天到分娩,一半的大鼠(无论是否摄入乙醇)饮用水中含有氯化镉(CdCl₂;50 ppm)。分娩当天,镉在母鼠的骨骼(7.3微克/克组织,湿重;与对照组相比,此值及其他值P < 0.05)、肝脏(12.9微克/克)和肾脏(13.0微克/克)中蓄积至中等水平,而大脑中的镉含量仅较低(0.45微克/克)。在6周龄的后代中,镉在大脑(34.0微克/克)、骨骼(15.9微克)、肾脏(78.2微克/克)尤其是肝脏(227.3微克/克)中大量蓄积。与镉同时给予的乙醇抑制了镉在大脑(1.8微克/克)、骨骼(3.28微克/克)和肾脏(61.3微克/克)中的蓄积,但增强了镉在肝脏(408.7微克/克)中的蓄积。在12周龄时,后代所有组织中的镉仅残留少量。这些发现表明两种已知致畸剂之间存在相互作用,乙醇可保护大脑免受镉蓄积。这种相互作用的性质尚不清楚,但可能与乙醇诱导肝脏和胎盘中的金属硫蛋白有关。

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