Iraqi Journal of Veterinary Sciences

This study was carried out to investigate the effect of induced prepubertal hyperthyroidism on the reproductive functions of male rats at the pubertal stage. Hyperthyroidism was induced by supplementing thyroxin in drinking water (0.002% w/v) and drenching of 200 μg/kg body weight. Sixty immature males (aged 50 days) were allocated to control and hyperthyroid (PH) groups, administered with distilled water and thyroxin, respectively. Each group was subdivided into three subgroups, sacrificed after 15 days (C15 and PH15), after administration for 15 days and left without treatment for 15 days (C15+ and PH15+), or after 30 days (C30 and PH30). After each period, body weight and relative weight of genital organs were recorded. Serum concentrations of thyroid stimulating hormone (TSH), thyroxin (TT4), triiodothyronine (TT3), follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone was assessed. The expression levels of testicular inha and thyroid hormone receptor (THR) genes were analyzed. Histopathological examination of testis was studied. Compared with control, PH group male rats showed decreased body weight gain and genital organ weights at all experimental periods, increased levels of serum TT4, TT3, and LH, decreased levels of TSH, FSH, and testosterone, and lower expression levels of testicular inha and THR genes. Testicular sections of PH group male rats, showed reduced germinal epithelium, vacuolation, and decreased the number of spermatocytes and Sertoli cells compared with control. In conclusion, the disturbed fluctuations of sex steroid hormones due to prepubertal hyperthyroidism might cause retardation of the testes’ development. 

The current study examined the association of thyroid disorders with reproductive dysfunction by determining its effect on gonadotropin secretion in cyclic female rats. Sixty cyclic females were assigned to three groups (20 each) and supplemented, for 30 days plus two consequent estrous cycles, with drinking water (control), methimazole in drinking water (0.02% w/v) (hypothyroid group), and thyroxine in drinking water (0.002% w/v) and gastric gavage of 200 μg/kg body weight (hyperthyroid group). At late proestrus, ten females from each group (for each cycle) were anesthetized and dissected. Blood samples were obtained to assess thyroid-stimulating hormone, free and total triiodothyronine, free and total thyroxin, follicle-stimulating hormone, luteinizing hormone, and prolactin concentrations. Ovarian and pituitary tissue samples were obtained for molecular analysis of ovarian thyroid receptor genes and pituitary TSH, FSHβ, and LHβ genes. In comparison with control, the Hypo group revealed increased serum concentrations of TSH and PRL and the expression levels of pituitary TSH and ovarian TRsTRs genes and significant decrease of FT3, TT3, FT4, TT4, FSH, and LHLH concentrations and the expression levels of pituitary FSHβ and LHβ genes. In contrast, the Hyper group showed increased serum FT3, TT3, FT4, TT4, and LHLH concentrations and the expression levels of pituitary LHβ and ovarian TRsTRs genes and decreased serum TSH FSH and PRL concentrations and pituitary FSHβ and TSH gene expression levels. It is concluded that thyroid dysfunction is associated with altered serum gonadotropin secretion and reproductive failure.