Prolonged exposure to hypoxia inhibits the growth of Pacific abalone by modulating innate immunity and oxidative status

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In aquatic animals, hypoxia is associated with growth retardation, impaired immunity, susceptibility to pathogens, oxidative stress, and mortality. However, the relative long-term effects of hypoxia on bivalves, including abalone, are not well understood. In this study, we examined the effects of exposure to hypoxic (2.5 and 4 mg O2 L−1) and normoxic (8 mg O2 L−1) conditions on the growth, survival, and immune and antioxidant responses of the economically important Pacific abalone Haliotis discus hannai over a 4 month period. We observed that exposure to 2.5 mg O2 L−1 resulted in marked reductions in assessed shell parameters, average meat weight, and survival compared with exposure to 4 and 8 mg O2 L–1. There were also significant reductions in oxygen consumption and ammonia-N excretion in abalone exposed to 2.5 mg O2 L−1. We also detected initial immunosuppression in the 2.5 mg O2 L−1-treated abalone, as evidenced by a significant reduction in total hemocytes and inhibition of antibacterial and lysozyme activities. Furthermore, intracellular malondialdehyde concentrations were significantly elevated at 1 month in the 2.5 mg O2 L−1 treatment group, whereas there were reductions in the levels of glutathione and enzymatic activities of catalase and superoxide dismutase, thereby indicating potential hypoxia-induced oxidative stress and a depression of antioxidant capacity. After 4 months of treatment, severe hypoxia (2.5 mg O2 L−1) had significantly modulated all measured parameters, whereas exposure to 4 and 8 mg O2 L−1 had induced no significant effects. Collectively, our observations indicate that under long-term exposure to hypoxia, Pacific abalone failed to maintain an effective antioxidant defense system and adequate immunity, with the observed biochemical disruptions leading to a reduction in growth and survival.