Antagonistic Effects Study Of Sodium Selenite On Mercury Chloride-Induced Myocardial Toxicity In Chickens

Mercury（Hg）is a kind of heavy metal with biological toxicity and widely consists in nature.Various forms of mercury can be enriched into livestock and poultry through the food chain,resulting in a decrease in their production performance.Selenium（Se）is an essential trace element for the organism,which plays a biological function in the form of selenoproteins.Meanwhile,Se can alleviate the toxicity of heavy metals.In recent years,it has been reported that Se alleviates tissue damage caused by heavy metals,but the mechanism of Se antagonizing Hg Cl₂ induced damage of chicken cardiac tissue remains unclear.Therefore,in this study,the antagonistic model of Na₂Se O₃against Hg Cl₂ injury in chicken myocardium was established to explore its mechanism.Ninety 1-day-old Hy-Line brown chicks were random Ly divided into Con group,Hg Cl₂ group,and Hg Cl₂+Se group,with 30 chicks in each group.The Con group was fed standard commercial rations and drinking water.The Hg Cl₂ group was fed standard commercial rations and drinking water supplemented with 250 mg/L Hg Cl₂.The Hg Cl₂+Se group was fed with a standard supplement of 10 mg/kg Na₂Se O₃ commercial diets and drinking water supplemented with 250 mg/L Hg Cl₂.All the chickens were executed after 7 weeks and myocardial samples were collected.The pathological changes of myocardial tissue injury were detected.HE staining was used to observe the pathological structural changes of chicken myocardial tissue.Use the commercial kit to detect the activities of serum enzymes creatine kinase（CK）,lactate dehydrogenase（LDH）,and oxidative stress indicators（MDA,T-SOD,and GSH-PX）.Western blotting（WB）was used to detect the protein expression levels of Ca²⁺channel related receptors（IP3R1,RYR2,PLN,SERCA2,STIM2,Orai1,CAMK2D,CAMK2G,NCX1,and PMCA）,endoplasmic reticulum stress related proteins（GRP78,PERK,e If2α,ATF4,ATF6,XBP1,and CHOP）,apoptosis related proteins（Bak1 and Caspase-3）,heat shock protein related proteins（HSP27,HSP40,HSP60,and HSP70）,and endoplasmic reticulum settled selenoproteins（SELENOK,SELENOM,SELENON,and SELENOS）.The Conclusions are as follows:Se alleviates the dissolution and reduction of chicken heart muscle fibers,inhibits the activities of serum enzymes CK and LDH,which indicate that Se alleviates the damage of chicken heart muscle tissue caused by Hg Cl₂ exposure.Se inhibits the up-regulation of Bak1 and Caspase-3 protein expression levels,which suggest that Se antagonizes the apoptosis of chicken myocardial tissue induced by Hg Cl₂exposure.Se increases the activity of antioxidant enzymes and decreases the content of MDA,which imply that Se antagonizes the oxidative stress of chicken myocardial tissue caused by Hg Cl₂exposure.Se inhibits the PERK-ATF4-CHOP pathway,which prove that Se alleviates endoplasmic reticulum stress in chicken cardiac tissue induced by Hg Cl₂ exposure.Se inhibits the up-regulation of HSP27,HSP40,HSP60,and HSP70 protein expression levels,which reveal that Se antagonizes the activation of heat shock protein in chicken cardiac tissue caused by Hg Cl₂ exposure.Se controls the expression of Ca²⁺related receptor proteins in cell membrane cytoplasm and endoplasmic reticulum,which expose that Se alleviates[Ca²⁺]_ER depletion and[Ca²⁺]_coverload in chicken cardiac tissue caused by Hg Cl₂ exposure.Se regulates the expression of endoplasmic reticulum settled selenoproteins,SELENOK,SELENOM,SELENON,and SELENOS,which show that Na₂Se O₃ alleviates the damage of chicken heart muscle tissue caused by Hg Cl₂ exposure.Conclusion:Se antagonizes Hg Cl₂-induced apoptosis of chicken myocardial tissue cells through relieving oxidative stress and endoplasmic reticulum stress induced by[Ca²⁺]_ERdeficiency.