- 著者
- Mostafa K. EL-AWADY Wael EL-GARF Lamia EL-HOUSSIENY
- 出版者
- The Japan Endocrine Society
- 雑誌
- Endocrine Journal (ISSN:09188959)
- 巻号頁・発行日
- vol.51, no.1, pp.37-46, 2004 (Released:2004-03-04)
- 参考文献数
- 44
- 被引用文献数
- 11 17
Testosterone and 5α-dihydrotestosterone (DHT) are the principal male hormones (androgens) in mammals. The enzyme, steroid 5α reductase catalyzes the conversion of testosterone (T) to its biologically potent steroid (DHT) in androgen dependent tissues. Two 5α reductase isoenzymes have been identified in rat tissues. The type I isoenzyme has been shown to be predominately expressed in the rat liver, whereas androgen target tissues of the genital tract express mainly isoenzyme II. The effects of androgens and glucocorticoids on the abundance of steroid 5α reductase type I (5αR1) messenger RNA in the rat liver were examined. Steady state levels of 5αR1 mRNA decreased dramatically to 1.5% of control levels 14 days following adrenalectomy (ADX), whereas dexamethasone (Dex) administered (0.5 mg/100 g) to ADX animals enhanced the expression of 5αR1 to twice its' normal values within 40 hours. Bilateral orchiectomy induced, within eight days, the expression of 5αR1 mRNA in the rat liver to 1.75 fold the normal value while testosterone injection failed to reduce this enhanced expression in castrated animals. Addition of Dex (1 μM) to primary cultures of rat hepatocyte resulted in a five- and three-fold reduction in the mRNA expression of 5αR1 after 24 and 48 hours, respectively. DHT (0.5 μM) however, induced the expression of 5αR1 mRNA by two- and seven-fold 24 and 48 hours post-treatment, respectively. In vitro nuclear run-on analysis of the 5αR1 gene showed no correlation between the rate of synthesis and steady state levels of this mRNA either in the intact liver or in cultured hepatocytes. These results appear to suggest that glucocorticoids and androgens differentially regulate 5αR1 mRNA in the rat liver. Moreover, our findings appear to indicate that regulation of 5αR1 gene is primarily at the post-transcriptional level.