Heat stress impairs growth and antioxidant-immune function in mandarin fish (Siniperca chuatsi) hepatic and mucosal tissues

This study aimed to elucidate the oxidative and immune mechanisms by which chronic heat stress induces multi-organ damage in mandarin fish ( Siniperca chuatsi ). Fish were exposed to a control (26 °C) and four high-temperature gradients (29 °C, 32 °C, 35 °C, and 38 °C). Compared to the control, heat stress at 32 °C and 35 °C significantly reduced growth performance and feed intake ( P < 0.05) without mortality, while 38 °C caused lethality. Heat stress disrupted tissue structure and antioxidant defenses, elevated serum cortisol, and reduced lysozyme and IgM levels ( P < 0.05). It also altered muscle quality by inducing lactic acid and malondialdehyde accumulation. In the gills and intestine, mucosal immune homeostasis was disrupted, as indicated by reduced activities of antioxidant enzymes (T-AOC, T-SOD, CAT) and increased expression of pro-inflammatory cytokines such as IL-1β, IL-8, and TNF-α ( P < 0.05). Critically, heat stress reprogrammed hepatic glycolipid metabolism via glycolysis and PPAR pathways and induced liver injury through ROS-dependent oxidative stress, which further triggered inflammation via MAPK pathway activation. These findings elucidate the physiological and immune responses of mandarin fish to extreme ambient temperatures and the molecular mechanisms of tissue oxidative damage under heat stress.