Li Yulong, Wang Hongbao, Wang Yanfei
College of Food and Bioengineering, Qiqihar University, Qiqihar, 161006, People's Republic of China.
College of Animal Science and Technology, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
Biol Trace Elem Res. 2024 Dec 4. doi: 10.1007/s12011-024-04470-4.
Cadmium (Cd), recognized as an environmental toxin, can cause injury to the testis in humans and animals. Oxidative stress (OS) can trigger an inflammatory response by promoting the activation of nuclear factor kappa beta (NF-κB) signaling pathway. Meanwhile, inflammation can lead to the occurrence of heat shock reaction. Yet, the specific mechanism by which Cd causes testicular injury in piglets, as well as the roles of oxidative stress, NF-κB signaling pathway, and heat shock response, still remained unclear. In this study, 6-week-old male piglets were selected as the experimental subjects, and the testicular injury model was developed by adding CdCl (20 mg/kg) to the feed. After 40 days, piglets were euthanized, and testis tissues were collected for the following experimental analysis (the ultrastructural characteristics, antioxidant levels, trace element concentrations, and molecular-level changes). The findings displayed that Cd exposure caused the widening of the perinuclear space and the fragmentation of the nuclear membrane in testis. In addition, Cd exposure increased the contents of Cd, iron (Fe), and manganese (Mn), while the contents of selenium (Se), calcium (Ca), zinc (Zn), and copper (Cu) were reduced in testis. The activities of oxidative enzymes inducible nitric oxide synthase (iNOS), hydrogen peroxide (HO), malondialdehyde (MDA), and nitric oxide (NO) were enhanced in testis after Cd exposure; meanwhile, the activities of antioxidant enzymes catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC) were reduced. And Cd exposure led to an upregulation of NF-κB, iNOS, interleukin 6 (IL-6), and cyclooxygenase-2 (COX-2) at both the mRNA and protein levels and increased the fluorescence intensity of the heat shock proteins (HSPs) HSP60, HSP70, and HSP90 in the testis. Altogether, Cd exposure induced toxic damage to piglet testis and potentially triggered inflammation through the oxidative stress/NF-κB signaling pathway and then resulted in heat shock response.
镉（Cd）被认为是一种环境毒素，可导致人类和动物的睾丸损伤。氧化应激（OS）可通过促进核因子κB（NF-κB）信号通路的激活引发炎症反应。同时，炎症可导致热休克反应的发生。然而，Cd导致仔猪睾丸损伤的具体机制以及氧化应激、NF-κB信号通路和热休克反应的作用仍不清楚。在本研究中，选择6周龄雄性仔猪作为实验对象，通过在饲料中添加CdCl₂（20 mg/kg）建立睾丸损伤模型。40天后，对仔猪实施安乐死，并采集睾丸组织进行以下实验分析（超微结构特征、抗氧化水平、微量元素浓度和分子水平变化）。结果显示，Cd暴露导致睾丸核周间隙增宽和核膜破裂。此外，Cd暴露增加了睾丸中Cd、铁（Fe）和锰（Mn）的含量，而硒（Se）、钙（Ca）、锌（Zn）和铜（Cu）的含量降低。Cd暴露后，睾丸中氧化酶诱导型一氧化氮合酶（iNOS）、过氧化氢（HO）、丙二醛（MDA）和一氧化氮（NO）的活性增强；同时，抗氧化酶过氧化氢酶（CAT）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GSH-PX）、超氧化物歧化酶（SOD）和总抗氧化能力（T-AOC）的活性降低。并且Cd暴露导致睾丸中NF-κB、iNOS、白细胞介素6（IL-6）和环氧化酶-2（COX-2）在mRNA和蛋白水平均上调，且睾丸中热休克蛋白（HSPs）HSP60、HSP70和HSP90的荧光强度增加。总之，Cd暴露诱导了仔猪睾丸的毒性损伤，并可能通过氧化应激/NF-κB信号通路引发炎症，进而导致热休克反应。
