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镉诱导鸡(Gallus domesticus)肝毒性及硒的缓解作用。

Cadmium induced hepatotoxicity in chickens (Gallus domesticus) and ameliorative effect by selenium.

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.

出版信息

Ecotoxicol Environ Saf. 2013 Oct;96:103-9. doi: 10.1016/j.ecoenv.2013.07.007. Epub 2013 Jul 29.

DOI:10.1016/j.ecoenv.2013.07.007
PMID:23906702
Abstract

Cadmium (Cd) is one of the most toxic metal compounds released into the environment. It was well known that Cd induced hepatotoxicity in animal models. However, little is known about the negative effects of Cd toxicity in the liver of birds. To investigate the Cd hepatotoxicity in birds and the protective effects of selenium (Se) against subchronic exposure to dietary Cd, 100-day-old cocks received either Se (as 10mg Na2SeO3 per kg of diet), Cd (as 150mg CdCl2 per kg of diet) or Cd+Se in their diets for 60 days. Histological and ultrastructural changes in the liver, the concentrations of Cd and Se, the lipid peroxidation (LPO) and nitric oxide (NO) production, the activities of the antioxidants superoxide dismutase (SOD) and glutathione peroxidase (GPx), nitric oxide synthase (NOS) activities and apoptosis were determined. Exposure to Cd significantly reduced SOD and GPx activity, Se content in the liver tissue. It increased the LPO and NO production, the numbers of apoptotic cells and Cd concentration and caused obvious histopathological changes in the liver. Concurrent treatment with Se reduced the Cd-induced liver histopathological changes, oxidative stress, overexpression of NO and apoptosis, suggesting that the toxic effects of Cd on the liver is partly ameliorated by inorganic Se. Se supplementation also modified the distribution of Cd in the liver.

摘要

镉(Cd)是环境中释放的最有毒的金属化合物之一。众所周知,镉会在动物模型中引起肝毒性。然而,关于鸟类肝脏中镉毒性的负面影响知之甚少。为了研究鸟类的镉肝毒性以及硒(Se)对亚慢性饮食镉暴露的保护作用,100 日龄公鸡接受了以下处理:饮食中添加硒(作为 10mg/kg 饲料的 Na2SeO3)、镉(作为 150mg/kg 饲料的 CdCl2)或镉+硒,处理时间为 60 天。测定了肝脏的组织学和超微结构变化、镉和硒的浓度、脂质过氧化(LPO)和一氧化氮(NO)产生、抗氧化剂超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)活性、一氧化氮合酶(NOS)活性和细胞凋亡。暴露于镉会显著降低 SOD 和 GPx 活性以及肝脏组织中的硒含量。它会增加 LPO 和 NO 的产生、凋亡细胞的数量以及镉浓度,并导致肝脏明显的组织病理学变化。同时添加硒可减轻镉引起的肝组织病理学变化、氧化应激、NO 和细胞凋亡的过度表达,表明无机硒部分减轻了镉对肝脏的毒性作用。硒补充还改变了肝脏中镉的分布。

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