Abstract
Water temperature stands as a crucial environmental element, exerting an impact on the survival and growth of organisms in aquaculture. Heat stress poses a significant threat to the survival and aquaculture of the Hong Kong oyster Magallana hongkongensis (also known as Crassostrea hongkongensis), yet the underlying physiological and molecular mechanisms remain poorly understood. This study investigated the effects of elevated temperatures (35 °C and 37 °C) on survival, DNA damage, antioxidant enzyme activities, and gene expression related to apoptosis, inflammation, and heat shock proteins (HSPs) in M. hongkongensis. The median lethal temperature (LT50) of M. hongkongensis was determined to be 37.09 °C, with significant mortality observed at 35 °C compared with the control (29 °C). Antioxidant enzyme activities (SOD, CAT, and GPx) and T-AOC were up-regulated initially but exhibited divergent patterns under prolonged stress, indicating a temperature-dependent threshold for oxidative defense. Comet assay results also showed that heat stress induced severe DNA damage in hemocytes. Moreover, heat stress significantly up-regulated mRNA expression of apoptosis-related genes (Caspase-2, Caspase-8, Bax, and P53), inflammatory genes (TNF, p38-MAPK, and AP-1), and HSP family members (Hsp70, Hsp90, Hsp27, and Hsp68). The expression peaks of these genes were generally earlier and more pronounced at 37 °C, reflecting intensified cellular damage and protective responses. Collectively, this study demonstrates that M. hongkongensis employs integrated antioxidant, apoptotic, inflammatory, and HSP-mediated mechanisms to counteract heat stress, but temperatures exceeding 35 °C disrupt these defenses, leading to survival impairment. These findings provide critical insights into the heat adaptation strategies of M. hongkongensis and serve as a scientific foundation for developing sustainable aquaculture practices to mitigate summer heat stress.