Molecular mechanism of selenium against lead-induced apoptosis in chicken brainstem relating to heat shock protein, selenoproteins, and inflammatory cytokines

• Published in: Ecotoxicology and environmental safety 2024-03, Vol.272, p.116028-116028, Article 116028
• Main Authors: Chen, Dechun, Yu, Weikang, Hao, Zhiyu, Qiu, Minna, Cui, Jiawen, Tang, You, Teng, Xiaohua, Liu, Yuhao, Liu, Haifeng
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Brainstem; Chickens - metabolism; Cytokines - genetics; Heat-Shock Proteins - genetics; Humans; Inflammatory cytokine; Lead; Proto-Oncogene Proteins c-bcl-2; Selenium; Selenium - pharmacology; Selenoproteins; Selenoproteins - genetics; Selenoproteins - metabolism
• ISSN: 0147-6513; 1090-2414
• DOI: 10.1016/j.ecoenv.2024.116028

Extensive application of lead (Pb) brought about environmental pollution and toxic reactions of organisms. Selenium (Se) has the effect of antagonizing Pb poisoning in humans and animals. However, it is still unclear how Pb causes brainstem toxicity. In the present study, we wanted to investigate whether Se can alleviate Pb toxicity in chicken brainstems by reducing apoptosis. One hundred and eighty chickens were randomly divided into four groups, namely the control group, the Se group, the Pb group, and the Se/Pb group. Morphological examination, ultrastructural observation, relative mRNA expressions of genes on heat shock proteins (HSPs); selenoproteins; inflammatory cytokines; and apoptosis-related factors were investigated. The results showed that Pb exposure led to tissue damage and apoptosis in chicken brainstems. Furthermore, an atypical expression of HSPs (HSP27, HSP40, HSP60, HSP70, and HSP90); selenoprotein family glutathione peroxidase (GPx) 1, GPx2, GPx3, and GPx4), thioredoxin reductases (Txnrd) (Txnrd1, Txnrd2, and Txnrd3), dio selenoprotein famliy (diodothyronine deiodinases (Dio)1, Dio2, and Dio3), as well as other selenoproteins (selenoprotein (Sel)T, SelK, SelS, SelH, SelM, SelU, SelI, SelO, Selpb, selenoprotein n1 (Sepn1), Sepp1, Sepx1, Sepw1, 15-kDa selenoprotein (Sep15), and selenophosphate synthetases 2 (SPS2)); inflammatory cytokines (Interleukin 2 (IL-2), IL-4, IL-6, IL-12β, IL-17, and Interferon-γ (IFN-γ)); and apoptosis-related genes (B-cell lymphoma-2 (Bcl-2), tumor protein 53 (p53), Bcl-2 Associated X (Bax), Cytochrome c (Cyt c), and Caspase-3) were identified. An inflammatory reaction and apoptosis were induced in chicken brainstems after exposure to Pb. Se alleviated the abnormal expression of HSPs, selenoproteins, inflammatory cytokines, and apoptosis in brainstem tissues of chickens treated with Pb. The results indicated that HSPs, selenoproteins, inflammatory, and apoptosis were involved in Se-resisted Pb poisoning. Overall, Se had resistance effect against Pb poisoning, and can be act as an antidote for Pb poisoning in animals. •Pb-induced brainstems pathophysiological changes and ultrastructural damage.•Se alleviated Th1/Th2 imbalance and immunosuppression in chicken brainstem.•Se increased antioxidant capacity and prevented apoptosis.•Se can antagonize Pb poisoning.