17 -Estradiol Treatment Decreases Steroidogenic Enzyme Messenger Ribonucleic Acid Levels in the Rainbow Trout Testis

Abstract

In fish, estrogens are well known for their involvement in ovarian differentiation and have been shown to be very potent feminizing agents when administrated in vivo during early development. However, the mechanism of action of exogenous estrogens is poorly understood. We report here on the feminizing effects of estrogen treatment on the testicular levels of some steroidogenic enzyme messenger RNAs [mRNAs; cholesterol side-chain cleavage (P450scc), 17-hydroxylase/lyase (P450c17), 3β-hydroxysteroid dehydrogenase (3βHSD), 11β-hydroxylase (P45011β), and aromatase (P450aro)] in the rainbow trout, Oncorhynchus mykiss. Treatment was carried out by dietary administration of 17β-estradiol (E2; dosage of 20 mg/kg diet) to a genetically all male population. Steroidogenesis in the differentiating testis was demonstrated to be strongly altered by E2, as this treatment resulted in considerable decrease in P450c17, 3βHSD, and P45011β mRNAs after only 10 days of treatment. In contrast, P450scc and P450aro mRNA levels were unaffected by E2, with P450scc mRNA levels remaining unaltered and P450aro not stimulated by this feminizing estrogen treatment. To better characterize this E2 effect, the same treatment was applied on postdifferentiating males, and roughly the same expression pattern was detected with a considerable decrease in testicular P450c17, 3βHSD, and P45011β mRNAs and a significant, but reduced, decrease in P450scc mRNA. In the interrenal, these steroidogenic enzyme mRNAs were not significantly affected by this E2 treatment, except for a slight, but significant, decrease in P450scc mRNA. These results clearly demonstrate that estrogens have profound effects on testicular steroidogenesis and that they are acting specifically on the testis by decreasing mRNA steady state levels of many steroidogenic enzyme genes. The decrease in P45011β mRNA, and thus inhibition of the synthesis of testicular 11-oxygenated androgens, may be an important step required for the active feminization of these genetic males.