Arsenic Toxicity on Metabolism and Autophagy in Adipose and Muscle Tissues

Arsenic, a naturally occurring metalloid derived from the environment, has been studied worldwide for its causative effects in various cancers. However, the effects of arsenic toxicity on the development and progression of metabolic syndrome, including obesity and diabetes, has received less attenti...

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Veröffentlicht in:Antioxidants 2022-03, Vol.11 (4), p.689
Hauptverfasser: Ro, Seung-Hyun, Bae, Jiyoung, Jang, Yura, Myers, Jacob F, Chung, Soonkyu, Yu, Jiujiu, Natarajan, Sathish Kumar, Franco, Rodrigo, Song, Hyun-Seob
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Sprache:eng
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Zusammenfassung:Arsenic, a naturally occurring metalloid derived from the environment, has been studied worldwide for its causative effects in various cancers. However, the effects of arsenic toxicity on the development and progression of metabolic syndrome, including obesity and diabetes, has received less attention. Many studies suggest that metabolic dysfunction and autophagy dysregulation of adipose and muscle tissues are closely related to the development of metabolic disease. In the USA, arsenic contamination has been reported in some ground water, soil and grain samples in major agricultural regions, but the effects on adipose and muscle tissue metabolism and autophagy have not been investigated much. Here, we highlight arsenic toxicity according to the species, dose and exposure time and the effects on adipose and muscle tissue metabolism and autophagy. Historically, arsenic was used as both a poison and medicine, depending on the dose and treatment time. In the modern era, arsenic intoxication has significantly increased due to exposure from water, soil and food, which could be a contributing factor in the development and progression of metabolic disease. From this review, a better understanding of the pathogenic mechanisms by which arsenic alters metabolism and autophagy regulation could become a cornerstone leading to the development of therapeutic strategies against arsenic-induced toxicity and metabolic disease.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox11040689