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镉诱导的鸡脾脏淋巴细胞损伤及硒的改善作用:氧化应激和细胞凋亡机制

Cadmium-induced injury and the ameliorative effects of selenium on chicken splenic lymphocytes: mechanisms of oxidative stress and apoptosis.

作者信息

Liu Shuang, Xu Feng-ping, Yang Zi-jiang, Li Ming, Min Ya-hong, Li Shu

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.

出版信息

Biol Trace Elem Res. 2014 Sep;160(3):340-51. doi: 10.1007/s12011-014-0070-0. Epub 2014 Jul 18.

DOI:10.1007/s12011-014-0070-0
PMID:25035189
Abstract

Cadmium (Cd) is an important environmental pollutant present in soil, water, air, and food. Selenium (Se) can antagonize some metal element toxicity including Cd. To investigate the cytotoxicity of Cd and the protective effects of Se on bird immunocytes in vitro, chicken splenic lymphocytes with CdCl2 (10(-6) mol/L), Na2SeO3 (10(-7) mol/L), and the mixture (10(-7) mol/L Na2SeO3 and 10(-6) mol/L CdCI2) were incubated for 12, 24, 36, and 48 h, respectively. A high level of malondialdehyde (MDA) and reactive oxygen species (ROS) productions were observed in Cd treatment group; the activities of catalase (CAT), glutathione peroxidise (GSH-Px), superoxide dismutase (SOD), and the mitochondrial inner transmembrane potential (ΔΨm) were significantly lower in Cd treatment group than those in controls (P < 0.05 or P < 0.01). In contrast, Se significantly improved the activities of antioxidant enzymes and reduced MDA and ROS levels compared to Cd treatment alone group, although not restored to the levels of control group. The population of apoptosis cells demonstrated that Cd induces the apoptosis of chicken splenic lymphocytes; in addition, increased mRNA level of Bak, p53, caspase-3, caspase-9, and cytochrome c (Cyt c) and decreased Bcl-2, Bcl-xl, and CaM were observed in Cd treatment group. Se ameliorated ΔΨm and [Ca(2+)]i for mitochondria function restoring, and Se was able to modulate the expression of relative genes. In conclusion, concurrent treatment with Se reduced the Cd-induced morphological changes and oxidative stress, ion disorder, and apoptosis, suggesting that the toxic effects of Cd on the chicken splenic lymphocytes were partly meliorated by Se.

摘要

镉(Cd)是一种存在于土壤、水、空气和食物中的重要环境污染物。硒(Se)可以拮抗包括镉在内的一些金属元素的毒性。为了在体外研究镉的细胞毒性以及硒对鸟类免疫细胞的保护作用,分别用氯化镉(10⁻⁶mol/L)、亚硒酸钠(10⁻⁷mol/L)以及二者混合物(10⁻⁷mol/L亚硒酸钠和10⁻⁶mol/L氯化镉)孵育鸡脾脏淋巴细胞12、24、36和48小时。在镉处理组中观察到丙二醛(MDA)和活性氧(ROS)的高水平产生;镉处理组中过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)的活性以及线粒体跨膜电位(ΔΨm)显著低于对照组(P<0.05或P<0.01)。相比之下,与单独镉处理组相比,硒显著提高了抗氧化酶的活性并降低了MDA和ROS水平,尽管未恢复到对照组水平。凋亡细胞数量表明镉诱导鸡脾脏淋巴细胞凋亡;此外,在镉处理组中观察到Bak、p53、半胱天冬酶-3、半胱天冬酶-9和细胞色素c(Cyt c)的mRNA水平升高,而Bcl-2、Bcl-xl和钙调蛋白水平降低。硒改善了线粒体功能恢复所需的ΔΨm和[Ca²⁺]i,并且硒能够调节相关基因的表达。总之,硒的联合处理减少了镉诱导的形态变化、氧化应激、离子紊乱和凋亡,表明镉对鸡脾脏淋巴细胞的毒性作用部分被硒减轻。

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