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.

Coenzyme Q10 Activates the Antioxidant Machinery and Inhibits the Inflammatory and Apoptotic Cascades Against Lead Acetate-Induced Renal Injury in Rats

“…For example, Thangarajan et al (2018) have demonstrated that PbAc intoxication in rats alters Bax/Bcl-2 expression, thereby increasing cytochrome c liberate from the mitochondrial matrix in the brain. Zhu et al (2017) have found that PbAc decreased Bcl-2 protein and mRNA expression, and elevated Bax and caspase-3 protein and mRNA expression, thus inducing cell death in chicken brain tissues and embryonic neurocytes via the mitochondrial pathway. Furthermore, Liu et al (2016) have found that PbAc caused a disruption in the mitochondrial integrity, the discharge of cytochrome c, the activation of caspase-3, and apoptosis in rat proximal tubular cells.…”

Antioxidant Defence Systems and Oxidative Stress in Poultry Biology: An Update

“…High dietary fluorine was found to decrease TrxR activity in chicken serum and tissues [238]. Similarly, dietary lead was associated with a decreased TrxR activity in chicken brain [239]. Heat stress was shown to compromise the mitochondrial thioredoxin system including Trx2, TrxR2 and Prx3 in growing chickens and dietary curcumin can mitigate this detrimental effect [240].…”

Cognitive Impairment Induced by Lead Exposure during Lifespan: Mechanisms of Lead Neurotoxicity

“…Moreover, a recent study showed that Pb induces apoptosis via the mitochondria pathway in both chicken brain tissues and embryonic neurocytes. This heavy metal can decrease mRNA and protein expression of Bcl-2 (an anti-apoptotic protein) while increase mRNA and protein expression of p53, Bax, Cyt C, and caspase-3 [ 177 ].…”