The Study Of Selenium Deficiency On Cerebrum Tissue Injury In Chicken

Selenium deficiency was a common Nutritional and metabolic disease in animal husbandry. It mainly displayed pathological change including degenerative necrosis of muscle, pancreas and pancreas tissue with leachability disposition. It also induced grave nerve functional impairment.Now, there were lots of studies about the effect of selenium deficiency on histology change of nerve tissue injure but none on apoptosis and calcium homeostasis.Selenium deficiency disease model was copyed in chicken by feeding selenium deficiency forages. The deiodinase activity, antioxidative function, apoptosis, calcineurin activity, [Ca2+]i, and the expression level of PHGPx and GAP-43 mRNA in cerebra were detected. The results showed as follows:1. In experimental stage, alvine flux, dyskinesia and leachability disposition were observed in experimental group. The typical musculi skeleti degeneration and necrosis with cerebromalacia could be found in obduction. The selenium content of experimental group was lower than control one and normal structure of tissue absence. Organelles were damaged. The results indicated that selenium deficiency induced injury of morphosis on nerve tissue in chicken and disease model was copyed successfully.2. GSH-Px activity, GSH activity and PHGPx mRNA expression level were decreased which resulted in oxidative stress of brain tissue and formed a serise of pathological change. It constructed the pathological fundation of brain injury in chicken selenium deficiency.3. T3 and FT3 content were decreased and T4, FT4 and TSH content were increased in serum. 5′-ID activity was decreased in the cerebrium. These indicated that selenium deficiency could cause hypothyroidism and then affected brain tissue growth.4. It conformed that selemium deficiency could cause apoptosis of brain tissue by ultrastructural observation and TUNEL detection. It was one of mechanisms of encephalodialysis induced by selemium deficiency.5. Selenium deficiency caused increased of [Ca2+]i and decreased of CaN activity and expression level of GAP-43 mRNA.It resulted disbalance of Calcium homeostasis and disorder of neural development, reparation functional. These results offered clues for further investigating mechanism about brain injured.These findings indicated selenium decifiency could cause hypothyreosis, oxidative stress of brain tissue, calcium homeostasis disbalance, apoptosis of nerve cells and self-repairing capability decrease. It was one of mechanisms of tissue injury induced by selenium deficiency.