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ISSN: 2157-7609
Journal of Drug Metabolism & Toxicology
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Heavy Metal Toxicity and Therapeutics

Honglian Shi*

Pharmacology and Toxicology, University of Kansas, USA

*Corresponding Author:
Honglian Shi
Associate professor
Pharmacology and Toxicology
University of Kansas, USA
Tel: 785-864-6192
Fax: 785-864-5219
E-mail: [email protected]

Received date: September 26, 2013; Accepted date: October 05, 2013; Published date: October 08, 2013

Citation: Shi H (2013) Heavy Metal Toxicity and Therapeutics. J Drug Metab Toxicol 4:e120. doi: 10.4172/2157-7609.1000e120

Copyright: © 2013 Shi H. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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It has long been known that heavy metal ions could be toxic and carcinogenic. Many metals such as arsenic and chromium induce cellular damages and carcinogenesis by increasing free radical generation and lowering cellular antioxidative defense capacity [1]. Targets of redox signaling induced by metals has been suggested to be potential therapeutic interventions in metal-induced toxicity and carcinogenesis. Aluminum is a known risk factor for neurodegeneration such as those in Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. In the issue of volume 4 issue 4, Thirunavukkarasu et al. [2] reported aluminum and its salts extensively damaged nervous system and impaired learning and memory of rats. More interestingly, they demonstrated that Manasamitra vatakam (MMV), a berbo-minearal formulation, provided protection against aluminum-induced toxicity in the rats. Furthermore, MMV markedly increased synthesis and release of neurotransmitter 5-hydroxytryptamine and decreased the expression of apoptotic genes such as Bcl-2, Bcl-xL and and caspas-3.

Yet, it is not clear how MMV improves the level of 5-HT and apoptotic proteins in the rats exposed to aluminum. In addition, aluminum is known to cause oxidative stress. Does MMV effect on the antioxidative defense system? If so, how? Further investigation is needed to provide more insight to the mechanisms of MMV-mediated brain function improvement in neurodegeneration.


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