Improvement of dietary N-acetylcysteine on growth inhibition and intestinal damage induced by β-conglycinin in juvenile Chinese mitten crabs (Eriocheir sinensis)

Abstract

β-conglycinin is a major component of feed allergens that can cause inflammation and dysfunction of intestinal digestion and absorption in fish, but little is known in crab. This study investigated the mitigative effects of N-acetylcysteine (NAC) on growth inhibition and intestinal damage induced by β-conglycinin in juvenile Chinese mitten crabs (Eriocheir sinensis). All three experimental diets contained 70 g/kg β-conglycinin, but with three levels of NAC in each diet (0, 0.5 and 1 g/kg respectively). The control diet did not contain β-conglycinin nor NAC, but all four diets were isonitrogenous and isolipidic. Juvenile crab (3.06 ± 0.03 g) were respectively fed with these diets for eight weeks. Dietary inclusion of 1 g/kg NAC significantly improved crab survival and weight gain than those of the negative control, and showed no difference with the control group. The crabs fed diets containing β-conglycinin had lower glutathione and catalase activities but higher malondialdehyde in the intestine than those in the control group. Moreover, dietary β-conglycinin improved the level of histamine in the intestine and increased the activity of diamine oxidase in serum. The activities of lipase in hepatopancreas and trypsin in both hepatopancreas and intestine were restrained by β-conglycinin, while addition of NAC reversed these negative effects. The addition of NAC restored the impaired immunity and morphological structure of the intestine. Moreover, dietary NAC downregulated mRNA levels of pro-inflammatory factor genes (lipopolysaccharide-induced TNF-α factor, EsRelish and interleukin-2 enhancer-binding factor 2) while upregulated the structural integrity peritrophic membrane related gene expression levels (peritrophin-like gene, peritrophic 1 and 2). This study indicates that N-acetylcysteine is a useful feed additive to ameliorate the growth inhibition, intestinal oxidative damage and inflammation induced by β-conglycinin in crab diets.