Abstract
Selenium is an important trace element with certain antioxidant effects. Nano-selenium, as a novel selenium source, has the advantages of strong biological activity, high absorption efficiency, and low toxicity. The aim of the present study was to compare the protective effects of sodium selenite and nano-selenium on intestinal oxidative stress induced by hydrogen peroxide (H(2)O(2)) in mice. A total of 60 female mice were randomly divided into 6 groups with 10 replicates per group and 1 mouse per replicate (n = 10). The first three groups were as follows: the Control group (C), fed with basal diet; the sodium selenite group (SS), basal diet + 0.3 mg·kg(-1) sodium selenite; and the nano-selenium group (NS), basal diet + 0.3 mg·kg(-1) nano-selenium. The latter three groups (CH, SSH, NSH) were fed the same diet as the former three groups, but the last 10 days of the experiment were fed with drinking water containing 0.3% H(2)O(2) to induce oxidative stress. The results showed that under normal conditions, the supplementation with sodium selenite or nano-selenium decreased the spleen index of mice; sodium selenate up-regulates GPX3 expression in the ileum, and increases T-SOD in the colon of mice; and nano-selenium up-regulated GPX1 expression but decreased T-AOC in the jejunum. After drinking water treated with H(2)O(2), H(2)O(2) increased the expression of intestinal inflammatory factors and selenium proteins, such as IL-1β and SOD in jejunum, IL-1β, NF-κB, IL-10, TXNRD1, TXNRD2, GPX1, GPX3, GPX4, and CAT in ileum, and IL-1β and SOD in colon. At the antioxidant level, H(2)O(2) decreased T-AOC in the jejunum. In the H(2)O(2) treatment, sodium selenite and nano-selenium increased the ratio of VH to CD (VH/CD) in jejunum; sodium selenite up-regulated the expression of TXNRD1 in jejunum, down-regulated the expression of GPX3 in ileum, at the antioxidant level, decreased the T-SOD and T-AOC in colon, and increased the content of MDA in ileum; and nano-selenium down-regulated the expression of TXNRD1 in colon. At the same time, the expression of IL-1β, NF-κB, IL-10, TXNRD1, TXNRD2, GPX1, GPX4, and CAT can be restored to normal levels by selenium supplementation. According to the results, drinking H(2)O(2) induced intestinal oxidative stress in mice to a certain extent, and selenium supplementation mitigated the destructive effect of H(2)O(2) on the intestinal morphology of mice jejunum and restored the level of related inflammatory factors, and had a positive effect on antioxidants.