Heat stress (HS) is a major challenge in poultry production due to its negative effects on growth, metabolism, and redox balance. Excessive reactive oxygen species generated during HS contribute to oxidative damage, emphasizing the need for nutritional strategies that enhance antioxidant capacity. This study evaluated the effects of dietary L-cysteine supplementation on growth performance, carcass traits, hepatic redox-related gene expression, and ileal nutrient transporters in commercial broilers. A total of 1,080 Cobb500 chickens (d 28–35) were assigned to diets containing deficient (0%), control (0.3%), or excess (0.6%) L-cysteine and exposed to thermoneutral (TN; 25°C), pair-feeding (PF; 25°C), or cyclic HS (35°C for 12 h daily). As expected, HS adversely affected (P 0.05) any performance variable under HS. Hepatic cystathionine-β-synthase ( CBS ) expression increased under cysteine-deficient conditions, indicating enhanced endogenous cysteine synthesis via the transsulfuration pathway. In contrast, expression of glutamate-cysteine ligase catalytic subunit ( GCLC ), cysteine dioxygenase-1 ( CDO1 ), and glutathione synthetase ( GSS ) did not differ (P > 0.05) among dietary cysteine levels, suggesting similar glutathione synthetic capacity across treatments. Ileal nutrient transporters, including SGLT1, GLUT5, FATP1, FABP2, PEPT1 , and PEPT2 , exhibited variable expression patterns in response to diet and temperature, reflecting differences in feed intake and intestinal physiological adaptation. Overall, dietary L-cysteine did not mitigate HS-induced declines in performance. Increased CBS expression under cysteine deficiency suggests robust endogenous regulation of cysteine supply, and further studies integrating protein abundance and enzyme activity are needed to elucidate L-cysteine’s biological effects under HS.
Aryal et al. (Wed,) studied this question.