Bracken W M, Klaassen C D
Toxicol Appl Pharmacol. 1987 Feb;87(2):257-63. doi: 10.1016/0041-008x(87)90287-0.
The purpose of the present study was to determine the ability of various short-chain alcohols to induce metallothionein (MT) in the liver and to determine whether the induction results from a direct action of alcohol on liver or an indirect action mediated by zinc, glucocorticoids, or catecholamines. Mice were administered alcohol by gavage and hepatic MT was quantitated by the Cd-hemoglobin radioassay. Ethanol, methanol, isopropanol, and propanol increased MT content to seven to nine times that of control liver. In vitro, ethanol did not increase MT concentrations in rat hepatocyte cultures, indicating that the in vivo induction is not a direct effect of ethanol on the liver. Adrenergic blocking agents did not reduce the MT content of ethanol-treated mice, indicating that catecholamines are probably not involved in the MT induction. Corticosterone and zinc concentrations in plasma were increased in mice 1 hr after ethanol treatment. Corticosterone, given in vivo, was a less effective inducer of MT than was ethanol treatment. In conclusion, hepatic MT was increased by several alcohols, the induction was not due to direct action of alcohol on the liver, and while the mechanism of alcohol induction of MT is unclear, it may be due to an alteration in zinc and glucocorticoid homeostasis.
本研究的目的是确定各种短链醇诱导肝脏中金属硫蛋白（MT）的能力，并确定这种诱导是由酒精对肝脏的直接作用引起的，还是由锌、糖皮质激素或儿茶酚胺介导的间接作用引起的。通过灌胃给小鼠施用酒精，并通过镉 - 血红蛋白放射测定法对肝脏MT进行定量。乙醇、甲醇、异丙醇和丙醇使MT含量增加至对照肝脏的七至九倍。在体外，乙醇不会增加大鼠肝细胞培养物中的MT浓度，这表明体内诱导不是乙醇对肝脏的直接作用。肾上腺素能阻断剂不会降低乙醇处理小鼠的MT含量，这表明儿茶酚胺可能不参与MT的诱导。乙醇处理1小时后，小鼠血浆中的皮质酮和锌浓度升高。在体内给予皮质酮，其诱导MT的效果不如乙醇处理。总之，几种醇会增加肝脏MT，诱导并非由于酒精对肝脏的直接作用，虽然酒精诱导MT的机制尚不清楚，但可能是由于锌和糖皮质激素体内平衡的改变。
