Methionine Antagonizes Liver and Kidney Antioxidant Function Damage in Heat-Stressed Rex Rabbits

Heat stress triggers systemic oxidative stress that compromises physiological homeostasis. This study evaluated methionine's effects on hepatic and renal antioxidant capacity in heat-stressed Rex rabbits. Rabbits were divided into five groups (30 replicates/group): control (20-25 °C, basal diet), heat stress (HS, 30-34 °C, basal diet), and HS +0.15%, 0.3%, or 0.45% methionine-supplemented groups. After 21 days, serum, skin, liver, and kidney samples were analyzed for biochemical parameters, oxidative stress markers, and gene expression. Results showed that 0.15-0.3% methionine supplementation under heat stress increased methionine apparent digestibility and suppressed amino acid catabolism; decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels; reduced skin malondialdehyde (MDA) and elevated (MSRA) activity; attenuated hepatic central venous congestion and renal tubular vacuolization; enhanced hepatic superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities (0.3% group); and modulated antioxidant gene expression via Nrf2/HO-1 and Nrf2/NQO1 pathways. Pathological analysis confirmed reduced fibrosis and cellular damage in liver/kidney tissues. Optimal methionine supplementation (0.3%) effectively mitigated heat-induced oxidative organ damage by enhancing endogenous antioxidant defenses and regulating redox-sensitive signaling pathways. These findings provide a nutritional strategy for alleviating heat stress-related metabolic disorders in rabbits.