Endocrine regulation and methylation patterns of rat class I alcohol dehydrogenase in liver and kidney.
Endocrine regulation and methylation patterns of rat class I alcohol dehydrogenase in liver and kidney.
复制标题
大鼠肝、肾Ⅰ类乙醇脱氢酶的内分泌调节及甲基化模式。
DOI：
10.1007/978-1-4684-5901-2_30
复制
发表时间：
1991
影响因子：
--
通讯作者：
Dipple,KM
中科院分区：
文献类型：
--
作者：
Crabb,DW;Qulali,M;Dipple,KM
Alcohol dehydrogenase (ADH) is expressed in a tissue-specific fashion and its activity is modulated by several hormones. Class I ADH activity is largely confined to the liver, with considerably smaller levels in the kidney. Experiments with intact animals indicate that thyroid hormone and testosterone reduce the activity of the enzyme in liver (Mezey and Potter, 1981; Rachamin et al., 1980), and that estrogen and growth hormone increase the activity (Teschke et al., 1986; Mezey and Potter, 1979). In primary hepatocyte cultures, growth hormone produced an increase in ADH activity and mRNA levels, and dihydrotestosterone reduced the activity (Mezey et al., 1986a, 1986b; Potter et al., 1989). Certain hepatoma cell lines express low levels of ADH activity and mRNA, and these can be induced by exposure to glucocorticoids (Wolfla et al., 1988; Dong et al., 1988). The enzyme activity in the kidney is induced by androgens in the mouse (Felder et al., 1988) and by estrogen in the rat (Dembic and Sabolic, 1982). Although the effect of androgens in mouse kidney is known to be mediated by an increase in the transcription of the gene, the mechanism of the effect of estrogens in rat kidney has not been reported.
