Effects Of Selenium Deficiency On Endogenous Hydrogen Sulfide And Relative Producing Enzymes In The Liver Of Chicken

Selenium (Se) is an important microelement for human and animals. Dietary selenium deficiency can cause a range of diseases. Liver is a target organ of Se-deficiency in chicken. Hydrogen sulfide (H2S) is the third gaseous signaling molecule discovered after NO and CO in recent years, and participate in many systems to regulate physical activity. Studies have shown that endogenous H2S has a protective effect on liver. H2S is synthesized mainly by Cystathionine y-lyase (CSE), cystathionine β-synthase (CBS), and3-mercaptopyruvate sulfurtransferase (3-MST) in vivo. Concentration of endogenous H2S and the expression of related enzymes can be changed by many diseases. But the relationship between Se-deficiency and endogenous H2S is unclear.As the experiment animals, chicks were fed for15,25,35,45,55,65d by Se-deficiency forage respectively, the content of Se in control groups forage is0.15mg/Kg, and in Se-deficiency forage groups is0.033mg/Kg. In this study, coding sequences of CSE were cloned and the polyclonal antibody has been successfully prepared by the methods of molecular biology. The effect of Se-deficiency on H2S concentration and the expression of H2S-producing enzymes in the liver of chicks were investigated and the results showed as follows:1. In this study, fusion proteins of CSE were expressed in prokaryotic system. The polyclonal antibodies were prepared and antibody titer was about1:25600in New Zealand white rabbit.2. The H2S concentration was increased significantly by dietary Se-deficiency in liver of chick.3. The expression of H2S-producing enzymes (CSE, CBS,3-MST) and CSE protein was increased by dietary Se-deficiency in liver of chick.In summary, dietary Se-deficiency can lead to the increase of H2S concentration, the expression of CSE, CBS,3-MST mRNA and CSE protein, so H2S and its producing enzymes play an important role in the damage caused by Se-deficiency, this may be regulated by organism to protect liver from damage induced by Se-deficiency. The experiment may provide a scientific basis for the field of endogenous H2S and Se-deficiency.