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2000
Volume 32, Issue 24
  • ISSN: 0929-8673
  • E-ISSN: 1875-533X

Abstract

Background

The by-product of naturally occurring rock, soil with different agricultural and industrial processes contaminated groundwater with a toxic metalloid- Arsenic (As3+), which results in different toxicities within the human body and in developing fetus.

Aim

The present study emphasizes evaluating the presence of oxidative stress and excessive generation of reactive oxygen species (ROS) resulting in mitochondrial dysfunction and caspase activation followed by apoptosis due to arsenic-induced neurotoxicity along with epigenetic modifications at different molecular targets.

Methods

Published articles available on PubMed and Scopus were studied and summarized.

Results

The precise mechanism causing arsenic-induced neurotoxicity at a critical stage of brain development is still unknown, while increased oxidative stress led to mitochondrial dysfunctions which are known to play a prominent role in this. AMPK acts as a metabolic checkpoint and restores ATP levels through a different anabolic pathway in energy starvation. At the same time, arsenic-induced AMPK activation leads to autophagy and neuronal cell death.

Conclusion

This review summarized the molecular mechanisms involved in arsenic-induced neurotoxicity, which can help to develop suitable future ameliorative and therapeutic strategies.

© 2025 Bentham Science Publishers
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/content/journals/cmc/10.2174/0109298673315956240829094938
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Changes in Energy Dynamics in Arsenic Exposure based Neurotoxicity: A Comprehensive Review
Curr. Med. Chem. 32, 5008 (2025); https://doi.org/10.2174/0109298673315956240829094938
/content/journals/cmc/10.2174/0109298673315956240829094938
/content/journals/cmc/10.2174/0109298673315956240829094938
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  • Article Type:     Review Article
Keyword(s): Arsenic; metalloid; mitochondrial dysfunction; neurotoxicity; oxidative stress; reactive oxygen species

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