Abstract
Exposure to extreme temperature conditions such as occurs in certain occupations is known to induce male infertility. In humans and most of the mammals, it has been shown that whole-body heat stress (HS) decreases fertility and produces defective embryos. Hence, the present study aimed at gaining some insights into the mechanisms producing defects after HS. In the present study, 56 mature male Wistar rats were randomly categorized into eight groups (n = 7), including group 1: Control, groups 2: Bioactive peptides (BPs; 10.00 mg kg(-1)), groups 3, 4, and 5: Heat-stressed (37.00, 39.00, and 43.00 ˚C for 20 min, respectively), and groups 6, 7, and 8: Heat-stressed along with BPs (10.00 mg kg(-1)), respectively. All treatments were administered orally once per day. The HS was induced through the immersion of rat scrotums in a water bath. After 45 days, rats were sacrificed and left testes were removed, fixed, and used for histological and immunohistochemical studies. Harvested right testes were also used for oxidative stress assessments and molecular analyses. Heat stress increased testicular tissue damage, elevated oxidative stress and reactive oxygen species production, and increased germ cells apoptosis, p53 and caspase 3 expressions, and Bax/Bcl-2 ratio. Treatment with BPs as a substance with anti-oxidant properties ameliorated the damage caused by HS. The results of this study highlight the protective role of BPs in the reproductive tract under HS. Bioactive peptides may have potential function against testicular tissue oxidative stress and apoptosis.