Effect of methionine deficiency on oxidative stress and apoptosis in the small intestine of broilers

The aim of this study was to investigate the effects of methionine (Met) deficiency on antioxidant functions (in the duodenal, jejunal and ileal mucosa) and apoptosis in the duodenum, jejunum and ileum of broiler chickens. A total of 120 one-day-old Cobb broilers were divided into two groups and fed a Metdeficient diet and a control diet, respectively, for six weeks. The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), the ability to inhibit hydroxyl radicals, and glutathione (GSH) content were significantly decreased in the Met-deficient group compared to the control. In contrast, malondialdehyde (MDA) content was significantly higher in the Met-deficient group. As measured by terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'- triphosphate dUTP nick end-labelling (TUNEL) and flow cytometry (FCM), the percentages of apoptotic cells were significantly increased. In conclusion, dietary Met deficiency can cause oxidative stress and then induce increased apoptosis in the intestine. Oxidative stress contributes to intestinal apoptosis. This results in the impairment of local intestinal mucosal immunity due to oxidative stress and apoptosis in the small intestine. The results of this study provide new experimental evidence for understanding the negative effects of Met deficiency on mucosal immunity or the functions of other immune tissues.