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硒通过减轻氧化应激和自噬对镉毒性对鸡胰腺的保护作用。

The Protective Effect of Selenium on the Chicken Pancreas against Cadmium Toxicity via Alleviating Oxidative Stress and Autophagy.

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. 2018 Jul;184(1):240-246. doi: 10.1007/s12011-017-1186-9. Epub 2017 Oct 9.

DOI:10.1007/s12011-017-1186-9
PMID:28994040
Abstract

Cadmium (Cd) is a highly toxic heavy metal that can affect human and animal health. Selenium (Se) is an essential microelement that can protect various organs against toxic heavy metals. Although many studies have investigated the adverse effect of Cd in rats and several other animals, little is known regarding the mechanisms of Cd-induced autophagy in the chicken pancreas and the antagonistic effect of Se on Cd. In the current study, we fed chickens Se, Cd, or Se and Cd supplements to establish the Se and Cd interaction model and to measure the concentrations of Se and Cd in the chicken pancreas. The ultrastructure changes of the chicken pancreas were also observed, and we detected oxidative stress indexes in each group. The expression levels of autophagy-related genes were also examined. We found that Cd exposure could increase the concentration of Cd, the activities of total superoxide dismutase (T-SOD), catalase (CAT), and glutathione peroxidase (GSH-Px); and the total antioxidant capacity (T-AOC) content in the chicken pancreas. The protein expression levels of dynein, Beclin1, LC3-1, LC3-2, and Atg5 were increased and that of TOR was decreased under Cd exposure conditions. However, the changes induced by Cd were significantly alleviated by Se. This study suggested that Cd could accumulate in the chicken pancreas and lead to oxidative stress and autophagy. Se was shown to antagonize Cd toxicity though reducing Cd accumulation, alleviating oxidative stress, and inhibiting autophagy. This study revealed a concrete mechanism for the Se antagonism of Cd and might provide a new clue for the detoxification of Cd poisoning.

摘要

镉 (Cd) 是一种剧毒重金属,会影响人类和动物的健康。硒 (Se) 是一种必需的微量元素,可保护各种器官免受有毒重金属的侵害。虽然许多研究已经调查了 Cd 对大鼠和其他几种动物的不良影响,但对于 Cd 诱导的鸡胰腺自噬的机制以及 Se 对 Cd 的拮抗作用知之甚少。在本研究中,我们给鸡补充 Se、Cd 或 Se 和 Cd,以建立 Se 和 Cd 的相互作用模型,并测量鸡胰腺中 Se 和 Cd 的浓度。还观察了鸡胰腺的超微结构变化,并检测了每组的氧化应激指标。还检查了自噬相关基因的表达水平。我们发现 Cd 暴露会增加鸡胰腺中 Cd 的浓度、总超氧化物歧化酶 (T-SOD)、过氧化氢酶 (CAT) 和谷胱甘肽过氧化物酶 (GSH-Px) 的活性以及总抗氧化能力 (T-AOC) 的含量。在 Cd 暴露条件下,动力蛋白、Beclin1、LC3-1、LC3-2 和 Atg5 的蛋白表达水平增加,而 TOR 的蛋白表达水平降低。然而,Se 显著减轻了 Cd 引起的变化。这项研究表明,Cd 可以在鸡胰腺中积累,导致氧化应激和自噬。Se 通过减少 Cd 积累、减轻氧化应激和抑制自噬来拮抗 Cd 毒性。本研究揭示了 Se 拮抗 Cd 的具体机制,为 Cd 中毒的解毒提供了新线索。

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