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Reactive nitrogen species (RNS) can induce the chronic inflammation and insulin resistance while the Peroxinitrite ions (ONOOˉ), one of RNS, may result in the nitration and affect phosphorylation of tyrosine in proteins, which may be one of the mechanisms.Selenium, as an essential nutritional trace element for mammals,exerts its biological effect through selenoproteins which incorporate selenium in the form of one or more selenocysteine residues. Recently, it is suggested that selenium has an insulin-mimetic action in addition to antioxidation and improving immune function, however, the relationship among selenium, the diabetes, proteins nitration and phosphorylation remains elusive.In this paper, hepatoma HepG2 cells and diabetes rats were given ectogenous sodium selenite solution to investigate the changes of protein nitration and phosphorylation. The results are as follows:(1) In the HepG2 cells, after the supplement of 0 to 300 nM sodium selenite solutions, there was no significant difference in the cells viability, however, the supplementation of selenium could reduce the proteins, nitrition induced by ONOOˉ, compared with control cells, however, there were no regular changes of phosphorylation level.(2) When diabetes mice were supplemented with selenium, the blood glucose levels were decreased. The results further indicate that selenium has an insulin-mimetic action. Like HepG2 cells, selenium in vivo can also weaken the proteins nitration in liver, kindey and musical of diabetes mice. Similarly, there were complicated infulences to the protein phosphorylation.Possible mechanism was discussed. Inhibition of protein nitration may be related to the upregulation of selenoproteins, by scavenging of ONOOˉ, however, the infulence mechanism of selenium supplementation on protein phosphorylation needs further study.
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