Journal
CHEMOSPHERE
Volume 210, Issue -, Pages 76-84Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.chemosphere.2018.06.165
Keywords
Copper; Arsenic; Skeletal muscle; Oxidative stress; NF-kappa B/p53 axis
Categories
Funding
- National Natural Science Foundation of China [31672619]
- Fundamental Research Funds for the Central Universities [2572016EAJ5, 2572016AA44]
- National Key Research and Development Program of China [2017YFD0501702]
Ask authors/readers for more resources
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-kappa B et al.) and Th1 bias immune system, suggested that exposure to Cu or/and As induces inflammation via NF-kappa B 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-kappa B/p53 axis might lead to the impairment of immune-apoptosis cross talk in the present model. (C) 2018 Elsevier Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available