Wang Min, Wang Yueyue, Wang Size, Hou Lulu, Cui Zilin, Li Qi, Huang He
College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, People's Republic of China.
College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, People's Republic of China.
Sci Total Environ. 2023 Mar 10;863:160601. doi: 10.1016/j.scitotenv.2022.160601. Epub 2022 Dec 15.
Cadmium (Cd) is a common heavy metal pollutant, and one of the important target organs of its toxicity is the testis. Selenium (Se) has the ability to antagonize the toxicity of Cd. However, the mechanism of the alleviating effects of Se on Cd in chicken testis injury through oxidative stress, endoplasmic reticulum stress (ERS), and programmed necrosis remained unclear. To explore this, 80 7-day-old chickens were divided into the Control group, the Se group (1.00 mg/kg Se), the Cd group (150.00 mg/kg Cd), and the CdSe group. On the 30th and 60th days, serum and chicken testis tissue samples were collected for testing. The results showed that Cd exposure resulted in swelling and deformation of seminiferous tubules, and thinning of the seminiferous epithelium. The ROS and MDA increased, and the SOD, CAT, GSH, GSH-Px decreased. The expression of GRP78, PERK, IRE1, ATF6, CHOP, and JNK in the Cd group increased. The expression of TNF-α, TNFR1, RIP1, RIP3, MLKL, and PARP1 increased, while the expression of Caspase-8 decreased. Histopathological changes, oxidative stress, ERS, and programmed necrosis were improved after CdSe treatment. In conclusion, Se antagonized the toxicity of Cd, and Se could alleviate Cd-induced oxidative stress, ERS, and programmed necrosis in chicken testis.
镉（Cd）是一种常见的重金属污染物，其毒性作用的重要靶器官之一是睾丸。硒（Se）具有拮抗Cd毒性的能力。然而，Se通过氧化应激、内质网应激（ERS）和程序性坏死减轻Cd对鸡睾丸损伤的作用机制仍不清楚。为了探究这一问题，将80只7日龄鸡分为对照组、Se组（1.00 mg/kg Se）、Cd组（150.00 mg/kg Cd）和CdSe组。在第30天和第60天，采集血清和鸡睾丸组织样本进行检测。结果显示，Cd暴露导致生精小管肿胀变形，生精上皮变薄。活性氧（ROS）和丙二醛（MDA）增加，超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GSH-Px）减少。Cd组中葡萄糖调节蛋白78（GRP78）、蛋白激酶样内质网激酶（PERK）、肌醇需求酶1（IRE1）、活化转录因子6（ATF6）、C/EBP同源蛋白（CHOP）和c-Jun氨基末端激酶（JNK）的表达增加。肿瘤坏死因子-α（TNF-α）、肿瘤坏死因子受体1（TNFR1）、受体相互作用蛋白1（RIP1）、受体相互作用蛋白3（RIP3）、混合谱系激酶结构域样蛋白（MLKL）和聚（ADP-核糖）聚合酶1（PARP1）的表达增加，而半胱天冬酶-8（Caspase-8）的表达减少。CdSe处理后，组织病理学变化、氧化应激、ERS和程序性坏死均得到改善。综上所述，Se拮抗了Cd的毒性，并且Se可以减轻Cd诱导的鸡睾丸氧化应激、ERS和程序性坏死。
