PS9-9. Vitamin E and Glutamine Mitigate Heat Stress-induced Cellular Damage and Preserve Myogenesis in Bovine Muscle-derived Cells.

Abstract As heat stress disrupts redox balance and impairs muscle development, identifying effective nutritional interventions at the cellular level remains critical. This study investigated the effects of vitamin E and glutamine supplementation on the gene expression of heat shock proteins, antioxidant enzymes, apoptosis markers, and myogenesis-related genes in bovine skeletal muscle-derived cells (BSMC) from Hanwoo under heat stress (HS) conditions. BSMC were differentiated for 5 d and subsequently exposed to either a thermoneutral control (37 °C) or HS (41 °C) for 24 h. Under HS condition, cells were treated with varying concentrations of vitamin E (0.1, 1, 5, 10 µM) or glutamine (0.1, 1, 10, 20 mM). Statistical analyses were performed using the GLM procedure of SAS. HS significantly increased (P < 0.05) the mRNA expression of heat shock proteins (heat shock protein family B member 1 (HSPB1), heat shock protein family A member 1A (HSP1A1)), the antioxidant enzyme (glutathione peroxidase 1(GPX1)), apoptosis-related genes (F-box protein 32 (FBXO32), caspase 3 (CASP3)), and Myogenin (MYOG), while decreasing the expression of late-stage myogenesis markers (myogenic factor 6 (MYF6), myosin heavy chain 1 (MYH1)) compared with control, indicating impaired myogenic progression. However, vitamin E supplementation at 1 and 5 µM significantly increased GPX1 expression and decreased CASP3 expression (P < 0.05) compared with the 41 °C, 0 µM vitamin E treatment. Furthermore, vitamin E at these dosages significantly restored MYH1 expression (P < 0.05). Similarly, glutamine supplementation at 1, 10, and 20 mM significantly downregulated CASP3 expression and upregulated MYH1 expression, compared with the 41 °C, 0 µM glutamine treatment (P < 0.05). Both treatments did not alter the heat-induced upregulation of HSPB1, HSP1A1, or FBXO32. These findings suggest that vitamin E and glutamine may attenuate heat stress-induced cellular damage in BSMC by suppressing apoptotic signaling and preserving late-stage myogenesis, supporting their potential as nutritional strategies to mitigate heat stress-related impairment of bovine muscle development.