Protective Effects Of Sodium Nitrite On Alcohol-induced Acute Liver Injury In Mice

Nitrite is widly distributing in nature.Acute nitrite poisoning which can cause methemoglobinemia.Chronic nitrite poisoning, which possible cause carcinogenesis and deformations. As a result, nitrite hasbeen considered poison. Many beneficial effects of nitrite were appeared in literature since2005. Forexample, it could be used to reduce blood pressure, resist arteriosclerosis, protect cell from ischemiareperfusion. Nitrite also could prevent cardiovascular disease. The mechanism about effects of nitrite waspossible involve in protect mitochondria, and reduce peroxide. We bethink of alcohol cause damage to theliver implicated oxidative stress, nitrite may be have protective effects on alcohol-induced acute liver injuryby parity of reasoning.The purpose of the present study was to investigate the protection by sodium nitrite （SN） onalcohol–induced acute liver injury in mice. Forty40male C57bL/6mice were randomly divided into4groups: the control group, SN group, acute alcohol-induced liver injury group(4.5g.kg^-1, ip) and SNpreconditioning group (these animal were pretreatmented with SN(16mg.kg^-1, ip)for12h, and thenadministrated alcohol for6h). The liver index was determined and compared between groups. Colorimetrictechnique was performed to measure the serum alanine transaminase （ALT）, aspartate transaminase （AST）,liver superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, catalase （CAT） activities,malondialdehyde （MDA） content. The pathological index or cell apoptosis of liver tissue was assayed byH&E and TUNEL fluorometric staining, the expression of hypoxia-inducible factor-1α （HIF-1α） proteinwas detected by Western-blotting and immunohistochemistry staining.The results showed that pretreatment with low doses of SN produced the following changes:1,increase in liver tissue SOD, GSH-Px, CAT activities （P<0.01）,2, decrease in serum ALT, AST levels（P<0.01）,3, reduction of MDA content and apoptosis index in liver tissue treated with alcohol （P<0.01）,4,raising HIF-1α protein, compared with the alcohol–induced acute liver injury group. It is suggested thatpretreatment of SN weakens acute alcohol-induced hepatocyte necrosis and improves pathological changes,which may be partially mediated by increase in HIF-1α. Conclusions1. Pretreatment with sodium nitrite could protect from alcohol–induced acute liver injury in mice.2. The cell protection mechanism involve with that sodium nitrite pretreatment increased antioxidativestress and the expression of HIF-1α in alcohol–induced acute liver injury mice.