Enzymatic oxidation and reduction of C19-delta5-3beta-hydroxysteroids by hepatic microsomes. IV. Induction of DHA hydroxylases and aminopyrine N-demethylase in immature male rats by androgens.

The capacities of various C19 steroids for prematurely inducing the normal metabolic patterns of rat liver in adulthood (70 days old) have been studied with hepatic microsomes of 42-day-old males castrated on day 24, 30, 32, or 34 of life. Dehydroepiandrosterone 16alpha-hydroxylase activity was significantly reduced (P less than 0.05) by castration during this 10-day interval but the 7alpha- and 7beta-hydroxylases, the N-demethylation of aminopyrine, and cytochrome P-450 concentration were unaffected. Daily administration of testosterone stimulated the DHA 16-alpha- and 17beta-hydroxylases, aminopyrine N-demethylation, and increased the P-450 content, but suppressed the 7alpha-hydroxylase. These effects only appeared with more than 1 week of the continuous treatment. Testosterone was the most active of the androgens studied; dihydrotestosterone (DHT) increased the DHA 16alpha-hydroxylase to a lesser extent, but this steroid and etiocholanolone stimulated DHA 7alpha-hydroxylation; androsterone was totally ineffective. These data suggest that testosterone rather than DHT from pubertal testes plays a significant role in control of hepatic oxidative enzyme activities during puberty.