Selenium against lead-induced apoptosis in chicken nervous tissues via mitochondrial pathway

Abstract

To investigate alleviative effect of selenium (Se) on lead (Pb)-induced apoptosis in chicken nervous tissues, 7-day-old chickens were randomly divided into four groups. The control group was fed a standard diet and drinking water. In the Pb and Se/Pb groups, (CH₃OO)₂Pb was dissolved in drinking water. In the Se and Se/Pb groups, Na₂SeO₃ was put into the standard diet. Embryonic neurocytes were divided into the control, Se (containing Na₂SeO₃), Pb (containing (CH₃COO)₂Pb), and Se/Pb (containing Na₂SeO₃ and (CH₃COO)₂Pb) groups. The following contents were performed: Morphologic observation for 90 days in brain tissues and for 12, 24, 36, and 48 hours in embryonic neurocytes; and antioxidant indexes, messenger RNA (mRNA) expression of twenty-five selenoproteins, and mRNA and protein expression of five apoptosis-related genes for 30, 60, and 90 days in brain tissues and for 12, 24, 36, and 48 hours in embryonic neurocytes. The results indicated that Se alleviated Pb-caused morphological changes; the decrease of superoxide dismutase, glutathione peroxidase (GPx), GPx1, GPx2, GPx3, GPx4, thioredoxin reductases (Txnrd)1, Txnrd2, Txnrd3, iodothyronine deiodinases (Dio)1, Dio2, Dio3, selenoprotein (Sel)T, SelK, SelS, SelH, SelM, SelU, SelI, SelO, Selpb, selenoprotein (Sep)n1, Sepp1, Sepx1, Sepw1, 15-kDa selenoprotein, and selenophosphate synthetases 2, and B-cell lymphoma-2 (Bcl-2); the increase of malondialdehyde, p53, Bcl-2 associated X protein, cytochrome c, and Caspase-3. Pb had time-dependent effects on GPx4, SelM, and malondialdehyde in the brain tissues; and on SelU in the embryonic neurocytes. Our data demonstrated that Se alleviated Pb-induced apoptosis in the chicken nervous tissues via mitochondrial pathway.