Nicotine Delays Puberty In Male Rat

Abstract

Immature male albino rats, 30 days of age, were treated with 0.3 mg nicotine/100 g body weight either orally or intraperitoneally for 30 days. All the animals were autopsied on the 61 st day, by which time they were sexually mature. Testis, epididymis, seminal vesicle, prostate gland and vas deferens were dissected out, weighed, and processed for biochemical and histological studies. Weight of testis and accessory sex organs of nicotine treated group was significantly reduced. The total cholesterol content was increased while protein, DNA and RNA contents were decreased. The acid phosphatase content was also decreased whereas that of alkaline phosphatase was increased. The surface epithelial cell height of accessory sex organs was decreased along with secretory activity. No spermatozoan was observed in the cauda epididymis of intraperitoneal nicotine treated rats. The changes in the testis and accessory sex organs may be due to reduced output of pituitary FSH and LH which are important to initiate the spermatogenesis and steroidogensis. The absence of spermatozoa in the cauda epididymis and reduction in the activities of accessory sex organs indicates the delay caused by nicotine in the attainment of puberty.

Associations between early alcohol and tobacco use and prolonged time to puberty in boys

“…The oral administration of nicotine to prepubertal rats has also been demonstrated to reduce testicular and secondary sexual organ weight (seminal vesicles, epididymis, prostate gland and vas deferens), suggesting delayed reproductive development (Londonkar et al . ). Thus, the alcohol and tobacco‐related deviations from the expected physiology of pubertal development in laboratory animals suggest that delayed onset of puberty should be explored as a potential health‐related outcome of early substance use.…”

“…Chronic administration of ethanol to prepubertal rats alters several pubertal indices by reducing serum testosterone (Anderson et al 1987;Cicero et al 1990;Salonen et al 1992), testicular weight (Anderson et al 1987;Cicero et al 1990) and the growth of secondary sexual organs (seminal vesicles and epididymis) (Anderson et al 1987;Cicero et al 1990;Salonen et al 1992). The oral administration of nicotine to prepubertal rats has also been demonstrated to reduce testicular and secondary sexual organ weight (seminal vesicles, epididymis, prostate gland and vas deferens), suggesting delayed reproductive development (Londonkar et al 2000). Thus, the alcohol and tobacco-related deviations from the expected physiology of pubertal development in laboratory animals suggest that delayed onset of puberty should be explored as a potential health-related outcome of early substance use.…”