Effect Of Sodium Selenite On Chicken Pancreas Injury Induced By Mercuric Chloride

Mercury（Hg）,a heavy metal element commonly known,is the only highly toxic heavy metal in liquid form at normal temperature and atmospheric pressure.The main forms of Hg exist in monomeric,inorganic,and organic forms.Mercury chloride（Hg Cl₂）is a widespread inorganic Hg that accumulates gradually in the body after entering the organism in various forms such as air,water,and food.In recent years,Hg pollution has become increasingly serious and the risk of Hg pollution of feed is increasing.The excessive enrichment of Hg in the poultry organism causes damage to organs due to the consumption of feed containing Hg.The pancreas is an important digestive gland in the animal body,and different types of heavy metal poisoning can cause serious damage to the structure and function of the pancreas.Selenium（Se）is an essential trace element in humans and animals that exerts its biological activity through selenoproteins and plays an important role in various biochemical pathways in the body.Se can antagonize tissue and organ damage caused by heavy metals,but whether Se can antagonize Hg Cl₂-induced pancreatic tissue damage in chickens and its specific mechanism are not clear yet.The study established a model of sodium selenite（Na₂Se O₃）antagonizing Hg Cl₂-induced pancreatic injury in chickens,and the mechanism of Se antagonizing Hg Cl₂-induced pancreatic injury in chickens was discussed from the perspective of oxidative stress,inflammation,and selenoproteins.Ninety 1-day-old male Hyland brown laying hens were randomly divided into three groups（30 chicken per group）:The Con group was fed with drinking water and standard commercial diets,the Hg Cl₂ group was fed drinking water containing Hg Cl₂（Hg Cl₂ content was 250 mg/L）and standard commercial diets,the Hg Cl₂+Se group was fed drinking water containing Hg Cl₂（Hg Cl₂ content was 250 mg/L）and standard commercial diets supplemented with sodium selenite（Na₂Se O₃ content was 10 mg/kg）.Pancreatic tissues and blood samples were sampled after 7 weeks for HE staining,serum biochemical analysis,oxidative stress index detection,quantitative real-time PCR（q RT-PCR）,and western blot（WB）.The results are as follows.1.The effect of Se on Hg Cl₂-induced pancreatic injury was investigated by HE staining and serum biochemical analysis.The results showed that Se alleviated Hg Cl₂-induced pancreatic hemorrhage,inflammatory cell infiltration,and pancreatic fibrosis.In addition,Se decreased the levels of Glu andα-AMY induced by Hg Cl₂.These results suggested that Se could alleviate the pathological and functional damage of pancreas caused by Hg Cl₂.2.MDA content and GSH-Px activity were measured by kits.The results showed that Se reversed the increase of MDA content and the decrease of GSH-Px activity in chicken pancreatic tissues caused by Hg Cl₂.These results suggested that Se could improve Hg Cl₂-induced oxidative stress in the pancreas.3.QRT-PCR and WB technology were applied to detect the m RNA and protein expression levels of inflammation-related genes in chicken pancreas.The results showed that Se inhibited the elevation of m RNA levels and protein levels related to inflammation（TNF-α,IL-1β,and IL-6）in chicken pancreatic tissues caused by Hg Cl₂.These results suggested that Se could inhibit inflammation in pancreatic tissues caused by Hg Cl₂.4.QRT-PCR and WB technology were applied to detect the m RNA and protein expression levels of related to pancreatic fibrosis,and WB technology was applied to detect the expression levels of proteins related to MAPK signaling pathway.The results showed that Se alleviated the Hg Cl₂-induced elevation of MAPK signaling pathway-related protein levels（p-p38 MAPK,p-JNK1/2,and p-ERK1/2）and pancreatic fibrosis-related m RNA and protein levels（TGF-β1,α-SMA,COL1A1,and FN1）in chicken pancreatic tissues.These results suggested that Se could alleviate Hg Cl₂-induced pancreatic fibrosis through MAPK signaling pathway.5.QRT-PCR and WB technology were applied to detect the m RNA and protein expression levels of selenoproteins in chicken pancreas.The results showed that Hg Cl₂ caused a decrease in the m RNA expression levels of some selenoproteins,including GPX2,GPX3,GPX4,TXNRD1,TXNRD2,TXNRD3,DIO1,SELENOF,SELENOH,SELENOI,SELENOK,SELENON,SELENOP,SELENOP2,SELENOS,SELENOT,SELENOW,SPS2,and MSRB1,and the addition of Se was able to significantly reverse this change.These results suggested that some selenoproteins were involved in the antagonistic effect of Se on Hg Cl₂-induced pancreatic toxicity.In conclusion,this study confirmed that Se could inhibit Hg Cl₂-induced oxidative stress and inflammation,and alleviate chicken pancreatic fibrosis through MAPK signaling pathway,as well as that some selenoproteins,especially those with antioxidant activity,were involved in the antagonistic effect of Se on Hg Cl₂ toxicity.