An increasing number of researches have been focused on the relationship between trace elements and animal health. Germanium, as a widely used trace element, exists ubiquitously as germanium or germanium compounds in the living environment of human and animals, and plays important roles in animal production or health. With the intensive study of the physiological function of germanium and its compounds, the effects of germanium on animal physiological functions and health have been gradually confirmed. In this review, we discuss the metabolic distribution, physiological characteristics, biological functions, germanium deficiency and germanium toxicity. Furthermore, we focus on the effects of germanium or germanium compounds on the immunity of animals. It is concluded that germanium or germanium compounds not only has positive effect but also has negative effect on animals. This review aims to provide a reference for the future research or application of the germanium or germanium compounds on animals or human beings.

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.

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