Combined effects of hypoxia and ammonia-N exposure ontheimmune response, oxidative stress, tissue injury and apoptosis of hybrid grouper (Epinephelus fuscoguttatus♀×E. lanceolatus♂).

Abstract

In order to investigate the simultaneous exposure to hypoxia and ammonia-N on oxidative stress, immune response, and apoptosis of the hybrid grouper, 120 healthy groupers were selected for hypoxia and/or ammonia-N exposure experiment. The fish were divided into four experimental groups: hypoxia and ammonia-N group, hypoxia group, ammonia-N group, and control group. The results demonstrated that ammonia-N and hypoxia exposures induced the superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities increased first and then decreased, and malondialdehyde (MDA) accumulated. Additionally, antioxidant genes (SOD, CAT, GSH-Px, HSP70, and HSP90), apoptosis genes (p53, bax, caspase 3, caspase 8, and caspase 9), and inflammatory genes (TNF-α, IL-1β, IL-6, and IL-8) were upregulated by hypoxia and ammonia-N exposure. Severe inflammatory features were noticed in fish under hypoxia and ammonia-N co-exposure and speculating that the p53-bax pathway may induce apoptosis in hybrid groupers. Furthermore, hybrid grouper exposed to hypoxia or ammonia-N revealed some abnormalities in liver histology, with combined exposure resulting in the most severe liver tissue lesions. In summary, the hypoxia and ammonia-N co-exposure induced oxidative stress, accelerating the cell damage and activated inflammation and apoptosis.