Heat stress and stocking density disrupt telomere maintenance through shelterin complex dysregulation and oxidative damage in broiler chickens.

BACKGROUND

Heat stress and high stocking density are major stressors in broiler chickens, compromising welfare and productivity. These stressors can induce oxidative damage and disrupt DNA structure, and potentially accelerate cellular aging. This study investigated the combined effects of heat stress and stocking density on telomere length, shelterin complex gene expression, and oxidative damage in broilers.

METHOD: A total of 198 male Ross 308 broilers were assigned to four groups: control (standard density, 10 birds/m²), heat (standard density + 38 °C), dense (high density, 17.5 birds/m²), and dense + heat (high density + 38 °C). At 42 days, liver tissues and blood were collected to measure telomere length, shelterin gene expression (TPP1, RAP1, POT1, TRF1, TRF2), and malondialdehyde (MDA) levels as an oxidative stress marker.

RESULTS

MDA levels increased significantly in heat and dense + heat groups compared to controls (P < 0.05), indicating elevated oxidative stress. Telomere length was reduced in all stressed groups (heat: -43.0%, dense: -21.5%, dense + heat: -38.7%; P < 0.05). Growth performance was compromised, with significant reductions in weight gain in the heat and dense + heat groups, and a higher feed conversion ratio in the dense + heat group (P < 0.05). POT1 and TPP1 gene expression was upregulated in stressed groups (P < 0.05), with the highest increase in dense groups (POT1: +282.4%, TPP1: +109.5%). No significant changes were observed in RAP1, TRF1, or TRF2 expression.

CONCLUSION

Heat stress and high stocking density disrupt telomere maintenance, likely through oxidative damage and dysregulation of shelterin components (POT1, TPP1). These findings highlight the need for improved management practices to mitigate stress-induced cellular damage in broiler production.