Heat Stress Alters Oxidative and Inflammatory Responses in Many Tissues of Male Rats

Objective: High ambient temperature beyond the comfort zone causes environmental heat stress (HS). A large number of free radicals are produced as a response to stress. This situation can cause morbidity and mortality in humans and animals. The current study was conducted to determine the effects of HS on antioxidant status, immune response and related factors. Methods: In the study, 18 Sprague Dawley male rats were used as animal materials. Rats were randomly assigned to Thermo-neutral group (TN; untreated at normal ambient temperature of 24 +/- 2 degrees C), Heat-stress 1 group (HS1; 8 hours daily exposure at 30 degrees C) and Heat-stress 2 group (HS2; 8 hours daily exposure at 35 degrees C). At the end of HS application (day 14), rats were sacrificed under ether anesthesia and brain, duodenum, heart, liver, thyroid and testis tissues were taken. The biochemical and inflammatory responses of the tissues were analyzed with the ELISA Kit. Results: Compared to the control group; Myeloperoxidase activity was higher in the heart tissue of HS2 group (p<0.05). Superoxide dismutaz activity was higher in the brain and testis tissues in HS2 group (p<0.05). Interleukin (IL)-2 level was higher in the duodenum and testis tissue of HS1 group and lower in the liver tissue (p<0.05). IL-6 level was higher in the brain and heart tissue of HS2 group (p<0.05). Tumor necrosis factor-alpha concentration was lower in the brain tissue in HS1 group, higher in the duodenum tissue in HS2 group and testicular tissue in HS1 group (p<0.05). Conclusion: These results showed that HS adversely affected the oxidant/antioxidant status of brain, heart and testis tissues of rats and immune response of brain, duodenum, heart, liver and testis tissues; also showed that the negative effects of exposure to HS were related to the severity of the stress in the heart, liver and testicular tissues.