Dietary rosemary oil alleviates heat stress-induced structural and functional damage through lipid peroxidation in the testes of growing Japanese quail

Supplementation of natural antioxidants to diets of male poultry has been reported to be effective in reducing or completely eliminating heat stress (HS)-induced reproductive failures. In this study, the aim is to investigate whether rosemary oil (RO) has a protective effect on HS-induced damage in spermatozoa production, testicular histologic structures, apoptosis, and androgenic receptor (AR) through lipid peroxidation mechanisms in growing Japanese quail. Male chicks (n = 90) at 15-days of age were assigned to two groups. The first group (n = 45) was kept in a thermo-neutral (TN) room at 22 °C for 24 h/d. The second group (n = 45) was kept in a room with a greater ambient temperature of 34 °C for 8 h/d (from 9:00 AM to 5:00 PM) and 22 °C for 16 h/d. Animals in each of these two groups were randomly assigned to three subgroups (RO groups: 0, 125, 250 ppm), consisting of 15 chicks (six treatment groups in 2 × 3 factorial design). Each of subgroups was replicated three times with each replicate including five chicks. The HS treatment significantly reduced the testicular spermatogenic cell counts, amount of testicular Bcl-2 (anti-apoptotic marker) and amount of AR. In addition, it significantly increased testicular lipid peroxidation, Bax (apoptotic marker) immunopositive staining, and the Bax/Bcl-2 ratio in conjunction with some histopathologic damage. Dietary supplementation of RO to diets of quail where the HS treatment was imposed alleviated HS-induced almost all negative changes such as increased testicular lipid peroxidation, decreased numbers of spermatogenic cells, and decreased amounts of Bcl-2 and AR, increased ratio of Bax/Bcl-2 and some testicular histopathologic lesion. In conclusion, dietary supplementation of RO for growing male Japanese quail reared in HS environmental conditions alleviates the HS-induced structural and functional damage by providing a decrease in lipid peroxidation.