The Regulatory Role of CgALDH6A1 in the Oxidative Stress Response of Crassostrea gigas Under High-Temperature Stress

High temperatures induce oxidative stress and the production of a large amount of malondialdehyde (MDA) in the Pacific oyster <i>Crassostrea gigas</i>, and they can even lead to mass mortality. Aldehyde dehydrogenase (ALDH) degrades MDA and is attracting increasing attention for its role in enhancing antioxidant defense capacity. This study identified 14 ALDH family members in the oyster genome. Among them, <i>Cg</i>ALDH6A1 harbored a conserved ALDH_F6_MMSDH domain (known to catalyze the oxidation of aliphatic and aromatic aldehydes) and was likely involved in the high-temperature stress response through the detoxification of accumulated toxic aldehydes. In the gills, <i>Cg</i>ALDH6A1 had significantly higher mRNA expression than other tissues, with a significant increase at 12 h under 28 °C high-temperature stress. During the outdoor aquaculture period, the mRNA transcripts of <i>Cg</i>ALDH6A1 in the gills exhibited a significant increase from June to October. After the expression of <i>Cg</i>ALDH6A1 was inhibited by RNAi, the MDA content in the gills increased significantly (1.31-fold, <i>p</i> < 0.01), while the activities of superoxide dismutase (SOD) (0.93-fold, <i>p</i> < 0.05) and catalase (CAT) (0.45-fold, <i>p</i> < 0.001) and total antioxidant capacity (T-AOC) (0.54-fold, <i>p</i> < 0.01) decreased significantly under high-temperature stress. Meanwhile, the gill tissue was observed to be disorganized with obvious filament swelling. After the oysters were treated with <i>Cg</i>ALDH6A1 agonist (Alda-1), the MDA content (0.59-fold, <i>p</i> < 0.001) in the gills decreased significantly, while the activities of SOD (1.33-fold, <i>p</i> < 0.001), CAT (1.81-fold, <i>p</i> < 0.001), and T-AOC (1.79-fold, <i>p</i> < 0.01) all increased significantly 48 h after high-temperature stress. However, no obvious morphological changes were observed in the gills. These results demonstrate that <i>Cg</i>ALDH6A1 plays a key role in regulating the oxidative stress response by degrading MDA under high-temperature stress and plays a cooperative role with the antioxidant system in alleviating oxidative stress under high-temperature stress.