College of Veterinary Medicine, Northeast Agricultural University, Harbin, P.R. China.
Chifeng Animal Health Supervision Institute, P.R. China.
J Nutr Biochem. 2022 Jul;105:108992. doi: 10.1016/j.jnutbio.2022.108992. Epub 2022 Mar 22.
Selenium (Se), a nutritionally essential mineral for humans and animals, has a significant antagonistic effect on heavy metal cadmium (Cd) biotoxicity. Still, the impact of different Se sources on alleviating Cd toxicity has received only limited attention. Therefore, the purpose of the current study was to assess the mitigation level of Cd-induced cardiotoxicity by different sources such as nanoparticles of Se, Se-rich yeast, and sodium selenite (SS). The results evidenced that the presence of Cd led to a significant increase in biochemical parameters such as lactate dehydrogenase and creatine kinase, as well as histopathological lesions in the heart of chickens. Cd exposure also resulted in more extensive effects on phase I metabolism enzymes and transcript cytochrome P450 isoforms, elevated the levels of malondialdehyde (MDA), glutathione (GSH), and hydrogen peroxide (HO) and depressed total superoxide dismutase (T-SOD), copper-zinc SOD (Cu-Zn SOD), total antioxidant capacity (T-AOC) and catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione-S-transferase (GST) activities. The expression of nuclear receptors, aryl hydrocarbon receptor (AHR), constitutive androstane receptor (CAR), and pregnane X receptor (PXR) was declined, down-regulated nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream targets in the Cd-treat group. Notably, Se sources application alleviated Cd toxicity by triggering AHR/CAR/PXR/Nrf2 signaling pathway to promote restoring antioxidant defense system and phase I metabolism enzymes system. However, when compared to the effectiveness of antagonism, the nanoparticles of Se were superior in relieving Cd-induced cardiotoxicity via AHR/CAR/PXR/Nrf2 pathway activation than other Se-sources.
硒（Se）是人类和动物必需的营养矿物质，对重金属镉（Cd）的生物毒性有显著的拮抗作用。然而，不同硒源缓解 Cd 毒性的影响还没有得到广泛关注。因此，本研究旨在评估纳米硒、富硒酵母和亚硒酸钠（SS）等不同硒源对缓解 Cd 诱导的心脏毒性的缓解程度。结果表明，Cd 的存在导致鸡心脏中乳酸脱氢酶和肌酸激酶等生化参数显著增加，同时出现组织病理学损伤。Cd 暴露还对 I 相代谢酶和细胞色素 P450 同工型转录物产生更广泛的影响，导致丙二醛（MDA）、谷胱甘肽（GSH）和过氧化氢（HO）水平升高，同时总超氧化物歧化酶（T-SOD）、铜锌超氧化物歧化酶（Cu-Zn SOD）、总抗氧化能力（T-AOC）和过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）和谷胱甘肽-S-转移酶（GST）活性降低。核受体芳香烃受体（AHR）、组成型雄烷受体（CAR）和孕烷 X 受体（PXR）的表达下降，Cd 处理组核因子红细胞 2 相关因子 2（Nrf2）及其下游靶基因下调。值得注意的是，硒源的应用通过激活 AHR/CAR/PXR/Nrf2 信号通路来促进抗氧化防御系统和 I 相代谢酶系统的恢复，从而缓解 Cd 毒性。然而，与拮抗作用的效果相比，纳米硒通过激活 AHR/CAR/PXR/Nrf2 途径缓解 Cd 诱导的心脏毒性的效果优于其他硒源。
