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Copper (II) and/or arsenite-induced oxidative stress cascades apoptosis and autophagy in the skeletal muscles of chicken
Chemosphere ( IF 8.1 ) Pub Date : 2018-05-11 , DOI: 10.1016/j.chemosphere.2018.05.013
Yu Wang , Hongjing Zhao , Yizhi Shao , Juanjuan Liu , Jinglun Li , Liyang Luo , Mingwei Xing

Arsenic (As) is a ubiquitous environmental toxin and robust inducer of oxidative stress (OxS). Copper (Cu) is an essential microelement, which participates in OxS as a cofactor for certain enzymes, with narrow optimal range between essential and toxic concentrations. However, their effects are rarely studied in chicken skeletal muscles, which have soaring per capita consumption andare susceptible to oxidative damage. In the present study, we demonstrated that the administration of copper sulfate (300 mg kg−1) or arsenite (30 mg kg−1) individually or their co-administration leads to varying degrees of OxS in the skeletal muscles of chickens. Corresponding to the protein expression pattern, the mRNA levels of caspase, B-cell lymphoma-2 (Bcl-2) families, and autophagy-related genes were also reduced in the experimental groups, indicating the involvement of both apoptotic and autophagic cell death. Additionally, rampant mitochondrial fission caused the vicious cycle between imbalanced mitochondrial dynamics and OxS, thus tethering intracellular homeostasis. The abovementioned muscle damage and index anomalies were time dependent, and more deteriorated effects were observed in Cu2+ and arsenite co-administered groups than those in groups administered Cu2+ and arsenite alone. Intriguingly, in the studied skeletal muscles, namely wing biceps brachii and leg gastrocnemius, there were conspicuous differences in oxidative toxicity susceptibility, which needs further study. The present study showed that Cu and/or As induce oxidative damage in chicken skeletal muscles and discussed its mechanism in terms of apoptosis, autophagy, and mitochondrial dynamics, thus voicing concerns about poultry breeding areas cross-contaminated with Cu2+ and arsenite.



中文翻译:

铜和/或亚砷酸盐诱导的氧化应激在鸡骨骼肌中级联凋亡和自噬

砷(As)是一种普遍存在的环境毒素,是氧化应激(OxS)的强力诱导剂。铜(Cu)是必需的微量元素,它参与OxS作为某些酶的辅助因子,在必需浓度和毒性浓度之间的最佳范围狭窄。但是,很少有人研究鸡肉的骨骼肌的效果,因为鸡肉的人均消耗量猛增,并且容易受到氧化损伤的影响。在本研究中,我们证明了硫酸铜(300 mg kg -1)或亚砷酸盐(30 mg kg -1)的施用)单独使用或共同使用会导致鸡骨骼肌中不同程度的OxS。与蛋白质表达模式相对应,实验组中的半胱天冬酶,B细胞淋巴瘤2(Bcl-2)家族和自噬相关基因的mRNA水平也降低,表明凋亡和自噬细胞死亡均参与其中。此外,猖ramp的线粒体裂变导致线粒体动力学失衡与OxS之间的恶性循环,从而束缚了细胞内稳态。上述肌肉损伤和索引距平时间依赖性的,并且在Cu中观察到更多的劣化的效果2+和亚砷共同给药组比在组施用的Cu 2+和亚砷酸盐。有趣的是,在研究的骨骼肌中,即肱二头肌肱二头肌和腿腓肠肌,其氧化毒性敏感性存在明显差异,有待进一步研究。本研究表明,Cu和/或As诱导了鸡骨骼肌的氧化损伤,并从细胞凋亡,自噬和线粒体动力学方面探讨了其机理,从而表达了对被Cu 2+和亚砷石交叉污染的家禽繁殖区的担忧。

更新日期:2018-05-12
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