Chronic Heat Stress-Induced Alterations in Hormonal Profile (Corticosterone, T3, T4, TSH) and Oxidative Stress Markers (MDA, GSH, GPx) in Laboratory Rats

Abstract

Chronic heat stress disrupts neuroendocrine balance and promotes oxidative damage, yet the duration-dependence of simultaneous hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-thyroid (HPT) axis responses and antioxidant status remains poorly defined. This study quantified the effects of daily heat exposure (2, 4, or 8 h/day at 42°C for 21 days) on serum corticosterone, triiodothyronine (T3), thyroxine (T4), and thyroid-stimulating hormone (TSH), and on hepatic oxidative markers malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPx) in adult male Wistar rats. Thirty-two rats (180–220 g) were randomized into four groups (n = 8): control and three heat-stressed groups (HS-2, HS-4, HS-8). ELISA quantified hormones, and oxidative markers were measured spectrophotometrically; data were analyzed by one-way ANOVA with Tukey HSD and Pearson correlation. Heat stress produced duration-dependent endocrine and oxidative changes (p < 0.001). Corticosterone rose 3.5-fold, from 45.2 ± 4.1 to 158.7 ± 13.2 ng/mL in HS-8, whereas T3, T4, and TSH fell by 48%, 55%, and 57%, respectively. MDA increased 3.7-fold (2.14 ± 0.18 to 7.88 ± 0.61 nmol/mL), and GSH and GPx declined by 66% and 71%. Corticosterone correlated positively with MDA (r = +0.892) and negatively with GSH (r = −0.874); T3 correlated negatively with MDA (r = −0.861) and T4 positively with GPx (r = +0.847). Chronic heat stress, therefore, causes duration-dependent HPA-axis activation, HPT-axis suppression, and antioxidant depletion, and the tight hormone-redox coupling supports the use of combined hormonal-antioxidant biomarker panels for grading heat-stress severity.