Li Yulong, Wang Shu, Wang Yanfei
College of Food and Bioengineering, Qiqihar University, Qiqihar, 161006, PR China; College of Animal Science and Technology, Northeast Agricultural University, Harbin, 150030, PR China.
College of Chemistry and Chemical Engineering, Qiqihar University, Qiqihar, 161006, PR China.
Environ Pollut. 2025 Feb 1;366:125514. doi: 10.1016/j.envpol.2024.125514. Epub 2024 Dec 9.
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 CdCl. 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-κB) 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 (HO) and malondialdehyde (MDA) were increased. Additionally, Caspase 8 expression was decreased, whereas the expression of TLR4, NF-κB, FADD, RIPK1, RIPK3, MLKL and heat shock proteins (HSPs) were increased after Cd stimulation. We concluded that Cd-triggered TLR4/NF-κB signaling pathway and oxidative stress potentially promoted necroptosis in pig epididymis.
镉（Cd）可通过附睾损伤导致生殖功能障碍。然而，关于镉诱导附睾毒性损伤的具体分子机制鲜有报道。本研究建立了猪附睾镉中毒模型。将10只6周龄雄性仔猪分为两组。对照组饲喂基础日粮，镉组饲喂添加20mg/kg氯化镉的日粮。40天后，将所有仔猪安乐死，采集附睾组织检测形态学变化、微量元素含量、氧化应激（OS）参数、Toll样受体4（TLR4）/核因子κB（NF-κB）信号通路及坏死性凋亡标记基因。本研究表明，镉导致猪附睾中镉元素浓度升高。形态学观察显示，镉组猪附睾组织受损。镉降低了谷胱甘肽（GSH）、总抗氧化能力（T-AOC）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-px）的含量，但过氧化氢（HO）和丙二醛（MDA）的含量增加。此外，镉刺激后，半胱天冬酶8（Caspase 8）表达降低，而TLR4、NF-κB、FADD、RIPK1、RIPK3、混合谱系激酶结构域样蛋白（MLKL）和热休克蛋白（HSPs）的表达增加。我们得出结论，镉触发的TLR4/NF-κB信号通路和氧化应激可能促进了猪附睾的坏死性凋亡。
