Abstract

The present research aimed to investigate the protection of N-acetylcysteine (NAC) on T-2 toxin-induced toxicity in Chinese mitten crab (Eriocheir sinensis). Crabs (0.27 ± 0.00 g) were fed four different diets (Control, T-2, 0.05% NAC + T-2 and 0.1% NAC + T-2) for 8 weeks. The results showed that T-2 toxin decreased growth performance, and induced oxidative stress, immunodepression and apoptosis in juvenile crabs. Crabs with NAC had higher weight gain, specific growth rate and hepatosomatic index than those in the T-2 group. The 0.1% NAC elevated crab survival and oxygen consumption rate and decreased alanine transaminase and aspartate transaminase in the serum of crabs fed T-2 toxin. Reactive oxygen species and malonaldehyde levels of hemolymph and hepatopancreas in crabs fed NAC were significantly lower than those in the T-2 group, while glutathione peroxidase, total antioxidant capacity, γ-glutamylcysteine synthetase activities and glutathione content significantly increased with 0.1% NAC. Total hemocyte count, respiratory burst activity, total protein, acid phosphatase (ACP) in hemolymph and ACP, alkaline phosphatase (AKP) in hepatopancreas were significantly enhanced with 0.1% NAC. Phagocytosis and AKP in hemolymph were significantly enhanced with 0.05% NAC supplementation. Furthermore, the mRNA expressions of antimicrobial peptides (ALF1, ALF2, crustin-1 and crustin-2) and peroxinectin were up-regulated with NAC. Besides NAC down-regulated the mRNA expressions of Relish, lipopolysaccharide-induced TNF-alpha factor, caspase-3, caspase-8 and p53 genes, and the ratio of Bax to Bcl-2 in the hepatopancreas. Our findings indicate that dietary NAC could improve the growth performance and survival of juvenile Chinese mitten crab fed T-2 toxin. The 0.1% NAC could effectively alleviate oxidative stress, immunodepression and apoptosis induced by T-2 toxin.

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