More about the testosterone induction of kidney alcohol dehydrogenase activity in the mouse.

Abstract

NAD-dependent alcohol dehydrogenase (ADH) found in liver and kidney has been shown to be specified by the same autosomally inherited gene locus in the quail (Ohno et al., 1969) as well as in the trout (Hitzeroth et al., 1968). The available evidence indicates that the same holds true for the mouse (Ohno et al., 1970). Yet, while ADH in liver is made all the time, ADH in kidney appears to be made only in the presence of sex steroids. The present study made on Balb/c inbred mice showed the following: (1) In the case of liver, ADH activity slowly increases throughout prepubertal development and reaches the high adult level at the onset of puberty. At all stages of development, liver ADH activity remains impervious to the administration of testosterone and estradiol as well as to castration and adrenalectomy. (2) In the case of kidney, no ADH activity can be detected until the twelfth postnatal day and adult ADH activity can be abolished by castration and adrenalectomy. In short, at any stage in postnatal development, kidney ADH is made only in the presence of an inducer. Testosterone is considerably more potent than estradiol as an inducer. The initial steep rise in kidney ADH activity following testosterone administration can be halted by actinomycin D, suggesting that induction involves the removal of the transcriptional block. (3) When fully induced by testosterone, kidney ADH activity on a per milligram protein basis reaches a level which equals the liver ADH activity level of that particular developmental stage. This suggests that the difference in the status of the same ADH locus in these two organs lies strictly in the presence of a transcriptional and possibly a translational block in the kidney. (4) Although the prostates and the uterus are favorite target organs of testosterone and estradiol, respectively, no ADH activity was induced in these organs either by testosterone or estradiol.