The purpose of the present study was to evaluate the sensitivity of testicular steroidogenesis during pubertal development to inhibition by ethanol. In vivo and in vitro human chorionic gonadotropin (hCG)-stimulated steroidogenesis were examined in CFW mice as a function of age. Plasma androstenedione, testosterone, and dihydrotestosterone (DHT) increased from ages 23 to 60 days in control mice. Acute ethanol treatment (3 g/kg) yielded static levels of androstenedione (0.45 ± 0.03 ng/mL), testosterone (6.4 ± 0.56 ng/mL), and DHT (2.3 ± 0.18 ng/mL) from ages 23 to 60 days, 30 to 60 days, and 35 to 60 days, respectively, resulting in reduction of plasma androstenedione, testosterone, and DHT (P < 0.05) relative to control values, but not until ages 35, 50, and 45 days, respectively. A similar insensitivity of the prepubertal testis to ethanol was seen in vitro. Inhibition of in vitro androstenedione and testosterone accumulation was seen only after ages 26 and 45 days, respectively. The data indicate that testosterone production by the pubertal testis is relatively insensitive to direct inhibition by ethanol. Previous studies have shown that chronic ethanol treatment of adolescent mice delays testicular maturation. The present study suggests that if chronic ethanol-induced delayed testicular development were due to impaired steroidogenesis, such impairment would be secondary to reduced gonadotropin stimulation and/or due to a chronic, rather than an acute, effect of ethanol.
Bibliographical noteFunding Information:
Acknowledgements -- The authors thank Ms Jean Arndt for her help m the manuscnpt preparation This work was supported by NIH grant AA06604
- Acute ethanol effects
- In vivo steroidogenesis
- Male puberty