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Oxidative stress-induced skeletal muscle injury involves in NF-κB/p53-activated immunosuppression and apoptosis response in copper (II) or/and arsenite-exposed chicken

Zhao, Hongjing, Wang, Yu, Shao, Yizhi, Liu, Juanjuan, Wang, Sirui, Xing, Mingwei
Chemosphere 2018 v.210 pp. 76-84
adverse effects, altitude, apoptosis, arsenic, catalase, chickens, copper, diet, enzyme activity, glutathione peroxidase, heavy metals, immune system, immunosuppression, inflammation, lipid peroxidation, malondialdehyde, models, muscle development, oxidative stress, skeletal muscle, toxic substances, toxicity, transcription factor NF-kappa B
The adverse effects of environmental toxicants such as copper and arsenic occur due to the generation of reactive oxygen species. Recent study also reported that both copper (Cu) and arsenic (As) may alter muscle regeneration. In order to assess the toxic effects of copper and arsenic on chicken skeletal muscle, chickens were subjected by different toxicologically relevant concentrations of copper or arsenic and their combination in diets for 12 weeks. Upon comparative analysis, a significantly higher malondialdehyde (MDA) and hydroxy radical content were observed in Cu or/and As exposed chicken skeletal muscle, which confirmed the strong lipid peroxidation nature of these two heavy metals. In addition, the depleted activity of catalase and glutathione peroxidase suggested the strong association of copper and arsenic with oxidative stress. Moreover, the higher elevation of pro-inflammatory mediators (NF-κB et al.) and Th1 bias immune system, suggested that exposure to Cu or/and As induces inflammation via NF-κB mediated response pathway. These results further coincided with inflammatory infiltration and nuclear condensation. Further, the execution of apoptosis machinery were characterized by a considerably elevated pro-apoptotic response and apoptotic index. In conclusion, the increased p53 levels detected in Cu or/and As treated chickens suggest the possibility that the NF-kB/p53 axis might lead to the impairment of immune-apoptosis cross talk in the present model.