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Heavy metal induced oxidative stress & its possible reversal by chelation therapy.
Indian J Med Res. 2008 Oct; 128(4):501-23.IJ

Abstract

Exposure to heavy metals is a common phenomenon due to their environmental pervasiveness. Metal intoxication particularly neurotoxicity, genotoxicity, or carcinogenicity is widely known. This review summarizes our current understanding about the mechanism by which metalloids or heavy metals (particularly arsenic, lead, cadmium and mercury) induce their toxic effects. The unifying factor in determining toxicity and carcinogenicity for all these metals is the generation of reactive oxygen and nitrogen species. The toxic manifestations of these metals are caused primarily due to imbalance between pro-oxidant and antioxidant homeostasis which is termed as oxidative stress. Besides these metals have high affinity for thiol groups containing enzymes and proteins, which are responsible for normal cellular defense mechanism. Long term exposure to these metals could lead to apoptosis. Signaling components affected by metals include growth factor receptors, G-proteins, MAP kinases and transcription factors. Chelation therapy with chelating agents like calcium disodium ethylenediamine tetra acetic acid (CaNa(2)EDTA), British Anti Lewisite (BAL), sodium 2,3-dimercaptopropane 1-sulfonate (DMPS), meso 2,3-dimercaptosuccinic acid (DMSA) etc., is considered to be the best known treatment against metal poisoning. Despite many years of research we are still far away from effective treatment against toxicity caused due to exposure to heavy metals/metalloids. The treatment with these chelating agents is compromised with number of serious side-effects. Studies show that supplementation of antioxidants along-with a chelating agent prove to be a better treatment regimen than monotherapy with chelating agents. This review attempts a comprehensive account of recent developments in the research on heavy metal poisoning particularly the role of oxidative stress/free radicals in the toxic manifestation, an update about the recent strategies for the treatment with chelating agents and a possible beneficial role of antioxidants supplementation to achieve the optimum effects. We have selected only arsenic, lead, mercury and cadmium for this article keeping in view current concerns and literature available.

Authors+Show Affiliations

Division of Pharmacology & Toxicology, Defence Research & Development Establishment, Gwalior, India. sjsflora@hotmail.comNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

19106443

Citation

Flora, S J S., et al. "Heavy Metal Induced Oxidative Stress & Its Possible Reversal By Chelation Therapy." The Indian Journal of Medical Research, vol. 128, no. 4, 2008, pp. 501-23.
Flora SJ, Mittal M, Mehta A. Heavy metal induced oxidative stress & its possible reversal by chelation therapy. Indian J Med Res. 2008;128(4):501-23.
Flora, S. J., Mittal, M., & Mehta, A. (2008). Heavy metal induced oxidative stress & its possible reversal by chelation therapy. The Indian Journal of Medical Research, 128(4), 501-23.
Flora SJ, Mittal M, Mehta A. Heavy Metal Induced Oxidative Stress & Its Possible Reversal By Chelation Therapy. Indian J Med Res. 2008;128(4):501-23. PubMed PMID: 19106443.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Heavy metal induced oxidative stress & its possible reversal by chelation therapy. AU - Flora,S J S, AU - Mittal,Megha, AU - Mehta,Ashish, PY - 2008/12/25/entrez PY - 2008/12/25/pubmed PY - 2009/3/31/medline SP - 501 EP - 23 JF - The Indian journal of medical research JO - Indian J Med Res VL - 128 IS - 4 N2 - Exposure to heavy metals is a common phenomenon due to their environmental pervasiveness. Metal intoxication particularly neurotoxicity, genotoxicity, or carcinogenicity is widely known. This review summarizes our current understanding about the mechanism by which metalloids or heavy metals (particularly arsenic, lead, cadmium and mercury) induce their toxic effects. The unifying factor in determining toxicity and carcinogenicity for all these metals is the generation of reactive oxygen and nitrogen species. The toxic manifestations of these metals are caused primarily due to imbalance between pro-oxidant and antioxidant homeostasis which is termed as oxidative stress. Besides these metals have high affinity for thiol groups containing enzymes and proteins, which are responsible for normal cellular defense mechanism. Long term exposure to these metals could lead to apoptosis. Signaling components affected by metals include growth factor receptors, G-proteins, MAP kinases and transcription factors. Chelation therapy with chelating agents like calcium disodium ethylenediamine tetra acetic acid (CaNa(2)EDTA), British Anti Lewisite (BAL), sodium 2,3-dimercaptopropane 1-sulfonate (DMPS), meso 2,3-dimercaptosuccinic acid (DMSA) etc., is considered to be the best known treatment against metal poisoning. Despite many years of research we are still far away from effective treatment against toxicity caused due to exposure to heavy metals/metalloids. The treatment with these chelating agents is compromised with number of serious side-effects. Studies show that supplementation of antioxidants along-with a chelating agent prove to be a better treatment regimen than monotherapy with chelating agents. This review attempts a comprehensive account of recent developments in the research on heavy metal poisoning particularly the role of oxidative stress/free radicals in the toxic manifestation, an update about the recent strategies for the treatment with chelating agents and a possible beneficial role of antioxidants supplementation to achieve the optimum effects. We have selected only arsenic, lead, mercury and cadmium for this article keeping in view current concerns and literature available. SN - 0971-5916 UR - https://www.unboundmedicine.com/medline/citation/19106443/Heavy_metal_induced_oxidative_stress_&_its_possible_reversal_by_chelation_therapy_ L2 - https://www.lens.org/lens/search/patent/list?q=citation_id:19106443 DB - PRIME DP - Unbound Medicine ER -
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