Liu Lili, Yang Bingyou, Cheng Yupeng, Lin Hongjin
College of Pharmacy, Heilongjiang University of Chinese Medicine, Harbin, 150040, People's Republic of China.
Biol Trace Elem Res. 2015 Oct;167(2):308-19. doi: 10.1007/s12011-015-0314-7. Epub 2015 Mar 26.
The harmful influences of dietary cadmium (Cd) on the chicken kidney and the protective role of selenium (Se) against Cd-induced nephrotoxicity in the chicken are relatively unexplored subjects. The aim of this study was to investigate the ameliorative role of Se on the effects of Cd-induced oxidative stress, endoplasmic reticulum stress, and apoptosis in chicken kidneys. For this study, 100-day-old chickens received Se (as 10 mg Na2SeO3/kg dry weight of diet), Cd (as 150 mg CdCl2/kg dry weight of diet), or Cd + Se in their diets for 60 days. Then, the histopathological changes, Cd and Se contents, levels of oxidative stress, inducible nitric oxide synthase-nitric oxide (iNOS-NO) system activity, levels of endoplasmic reticulum (ER) stress, results of the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay of apoptosis, and expression levels of Bcl-2 and caspase 3 in the kidney were examined. The results showed that Cd exposure caused histopathological and ultrastructural damage and apoptosis of the kidneys. Cd administration significantly increased the accumulation of Cd, the malondialdehyde (MDA) content, NO production, iNOS activity, iNOS expression levels, expression levels of ER stress-related genes (GRP78, GRP94, ATF4, ATF6, and IRE) and the pro-apoptosis gene caspase 3, and the rate of apoptosis. Cd administration markedly decreased the Se content, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, and anti-apoptosis gene Bcl-2 expression levels. Co-treatment with Se and Cd obviously reduced the accumulation of Cd, Cd-induced histopathological and ultrastructural changes, oxidative stress, iNOS-NO system activity, ER stress, caspase 3 expression levels, and the rate of apoptosis in the kidneys. These results suggested that Cd exposure caused renal injury and that Se ameliorated Cd-induced nephrotoxicity in chickens.
膳食镉（Cd）对鸡肾脏的有害影响以及硒（Se）对鸡体内镉诱导的肾毒性的保护作用，是相对未被充分研究的课题。本研究的目的是探讨硒对镉诱导的鸡肾脏氧化应激、内质网应激和细胞凋亡的改善作用。在本研究中，100日龄的鸡在其日粮中分别摄入硒（以10 mg Na2SeO3/kg干重日粮的形式）、镉（以150 mg CdCl2/kg干重日粮的形式）或镉+硒，持续60天。然后，检查肾脏的组织病理学变化、镉和硒含量、氧化应激水平、诱导型一氧化氮合酶-一氧化氮（iNOS-NO）系统活性、内质网（ER）应激水平、细胞凋亡的末端脱氧核苷酸转移酶dUTP缺口末端标记（TUNEL）检测结果，以及肾脏中Bcl-2和半胱天冬酶3的表达水平。结果表明，镉暴露导致肾脏的组织病理学和超微结构损伤以及细胞凋亡。镉的摄入显著增加了镉的积累、丙二醛（MDA）含量、一氧化氮生成、iNOS活性、iNOS表达水平、内质网应激相关基因（GRP78、GRP94、ATF4、ATF6和IRE）的表达水平以及促凋亡基因半胱天冬酶3的表达水平和细胞凋亡率。镉的摄入显著降低了硒含量、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）活性以及抗凋亡基因Bcl-2的表达水平。硒和镉联合处理明显减少了镉的积累、镉诱导的组织病理学和超微结构变化、氧化应激、iNOS-NO系统活性、内质网应激、半胱天冬酶3表达水平以及肾脏中的细胞凋亡率。这些结果表明，镉暴露会导致肾损伤，而硒可改善镉诱导的鸡肾毒性。
