Studies Of The Antagonism Of Selenium On Aluminium-induced Reproductive Toxicity In Male Mice

Objective:The objective of this research was to detect aluminium-induced reproductive toxicity and antagonism of selenium on aluminium-induced reproductive toxicity by morphology,cytology and molecular level.This study was also to provide the evidences for the prevention arid treatment of reproductive toxicity induced by aluminium exposure.Methods:From different aspects,this essay approaches the reproductive toxicity of aluminium and the antagonistic effect of selenium on that in male mice by using chromosome aberration,single cell gel electrophoresis,sperm aberration,fluoresccnt staining sperm nucleus and pathological section of testis.Results:(1)Male reproductive toxicity induced by aluminum:the decreased variation of body weight as well as testicular weight were recorded in mice treated with aluminum alone, which was accompanied by an increase of rate of chromosome aberration,rate of sperm aberration and rate of immaturity sperm;CASP image analyze of comet assay shows that every analytic index of all dosage groups shows statistical significance compared with negative groups;pathological section of testis shows that aluminum can damage the structure of testis.(2)The antagonistic effect of selenium on aluminium-induced Reproductive Toxicity: Se given resulted in partial recovery of the reproductive parameters above studied (P＜0.05);furthmore the antagonistic effect of selenium is relevant to the dosage.the middle-dose Se is the optimization.Conclusion:(1)Aluminium trichloride exposure could damage testicle cell DNA and increase rate of chromosome aberration,rate of sperm aberration,rate of immaturity sperm and damage the structure of testis.(2)Selenium could antagonize partly aluminium -induced male reproductive toxicity.(3)The antagonistic effect of selenium is relevant to the dosage and object,0.2 and 0.4mg Na₂SeO₄/kg/d groups show the equivalent effect of antagonism on testicle cell, 0.4mg Na₂SeO₄/kg/d group possesses the optimal effect of antagonism on sperm damage.