The antagonistic effect of selenium on lead-induced apoptosis and necroptosis via P38/JNK/ERK pathway in chicken kidney

细胞凋亡 坏死性下垂 MAPK/ERK通路 p38丝裂原活化蛋白激酶 程序性细胞死亡 化学 信号转导 基因 肾毒性 细胞生物学 生物 生物化学 遗传学
作者
Zhiruo Miao,Zhiying Miao,Xu Shi,Hao Wu,Yujie Yao,Shiwen Xu
出处
期刊:Ecotoxicology and Environmental Safety [Elsevier BV]
卷期号:231: 113176-113176 被引量:85
标识
DOI:10.1016/j.ecoenv.2022.113176
摘要

Lead (Pb), as a toxic heavy metal pollutant, has been paid much attention. Pb is often discharged into the environment through the soot, wastewater and waste residue in industrial production, which poses a great threat to animal health. Selenium (Se) is a trace element known to antagonize the toxicity caused by heavy metals. However, the interaction between Se and Pb in chicken kidney and its specific biological mechanism are still unclear. So, we constructed chicken models of Pb exposure and Pb, Se co-exposure. Therefore, we used western blot and qRT-PCR to detect the expression of related genes. The results showed that Pb activated the MAPK signaling pathway by up-regulating the expression of MARK pathway genes to induce the expression of pro-apoptotic genes and necroptosis-related genes. Se can regulate the MARK signaling pathway and attenuated the expression of MAPK pathway genes altered by Pb to reduce apoptosis and necroptosis of chicken kidney cells. Our study gives new ideas for the specific mechanism of Pb nephrotoxicity and provides a reference for comparative medicine and clinical medication.
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