Cadmium exposure induces oxidative stress-mediated necroptosis via TLR4/NF-κB signaling pathway in pig epididymis

文献类型： 外文期刊

第一作者： Li, Yulong

作者： Li, Yulong;Wang, Yanfei;Wang, Shu;Li, Yulong

作者机构：

关键词： Cadmium; Pig epididymis; TLR4/NF-kappa B signaling pathway; Oxidative stress; Necroptosis

期刊名称：ENVIRONMENTAL POLLUTION （ 影响因子：7.3； 五年影响因子：8.1 ）

ISSN： 0269-7491

年卷期： 2025 年 366 卷

页码：

收录情况： SCI

摘要： Cadmium (Cd) can cause reproductive disorders through epididymal injury. However, the specific molecular mechanism of Cd-induced epididymal toxic injury is rarely reported. In this study, the model of Cd poisoning in pig epididymis was established. Ten 6-week-old male piglets were divided into two groups. The control group was fed a basic diet, while the Cd group received a diet supplemented with 20 mg/kg CdCl2. After 40 days, All piglets were euthanized, and epididymal tissues were collected to detect morphological changes, trace element contents, oxidative stress (OS) parameters, toll like receptor 4 (TLR4)/nuclear factor kappa-B (NF-kappa B) signaling pathway and necroptosis marker genes. This study showed that Cd led to an increased concentration of Cd element in pig epididymis. According to morphological observation, pig epididymal tissue in the Cd group was damaged. Cd decreased the contents of glutathione (GSH), total antioxidant capacity (T-AOC), catalase (CAT), dismutase (SOD), and glutathione peroxidase (GSH-px), but the contents of hydrogen peroxide (H2O2) and malondialdehyde (MDA) were increased. Additionally, Caspase 8 expression was decreased, whereas the expression of TLR4, NF-kappa B, FADD, RIPK1, RIPK3, MLKL and heat shock proteins (HSPs) were increased after Cd stimulation. We concluded that Cd-triggered TLR4/NF-kappa B signaling pathway and oxidative stress potentially promoted necroptosis in pig epididymis.

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