<abstract xml:lang="en" xmlns="http://www.w3.org/1999/xhtml"><p>Sulfur mustard (SM), also known as mustard gas, has been the most widely used chemical weapon. The toxicity of SM as an incapacitating agent is of much greater importance than its ability to cause lethality. Acute toxicity of SM is related to reactive oxygen and nitrogen species, DNA damage, poly(ADP-ribose) polymerase activation and energy depletion within the affected cell. Therefore melatonin shows beneficial effects against acute SM toxicity in a variety of manner. It scavenges most of the oxygen- and nitrogen-based reactants, inhibits inducible nitric oxide synthase, repairs DNA damage and restores cellular energy depletion. The delayed toxicity of SM however, currently has no mechanistic explanation. We propose that epigenetic aberrations may be responsible for delayed detrimental effects of mustard poisoning. Epigenetic refers to the study of changes that influence the phenotype without causing alteration of the genotype. It involves changes in the properties of a cell that are inherited but do not involve a change in DNA sequence. It is now known that in addition to genetic mutations, epimutations can also involve in the pathogenesis of a variety of human diseases. Several actions of melatonin are now delineated by epigenetic actions including modulation of histone acetylation and DNA methylation. Future studies are warranted to clarify whether epigenetic mechanisms are involved in pathogenesis of delayed sulfur mustard toxicity and melatonin alleviates delayed toxicity of this warfare agent.</p></abstract>

Sulfur mustard (SM), also known as mustard gas, has been the most widely used chemical weapon. The toxicity of SM as an incapacitating agent is of much greater importance than its ability to cause lethality. Acute toxicity of SM is related to reactive oxygen and nitrogen species, DNA damage, poly(ADP-ribose) polymerase activation and energy depletion within the affected cell. Therefore melatonin shows beneficial effects against acute SM toxicity in a variety of manner. It scavenges most of the oxygen- and nitrogen-based reactants, inhibits inducible nitric oxide synthase, repairs DNA damage and restores cellular energy depletion. The delayed toxicity of SM however, currently has no mechanistic explanation. We propose that epigenetic aberrations may be responsible for delayed detrimental effects of mustard poisoning. Epigenetic refers to the study of changes that influence the phenotype without causing alteration of the genotype. It involves changes in the properties of a cell that are inherited but do not involve a change in DNA sequence. It is now known that in addition to genetic mutations, epimutations can also involve in the pathogenesis of a variety of human diseases. Several actions of melatonin are now delineated by epigenetic actions including modulation of histone acetylation and DNA methylation. Future studies are warranted to clarify whether epigenetic mechanisms are involved in pathogenesis of delayed sulfur mustard toxicity and melatonin alleviates delayed toxicity of this warfare agent.

Acute and delayed sulfur mustard toxicity; novel mechanisms and future studies

Department of Physiology, School of Medicine, Gulhane Military Medical Academy, Ankara, Turkey

Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA

Interdisciplinary Toxicology

{"article-title":"Acute and delayed sulfur mustard toxicity; novel mechanisms and future studies"}

Sulfur mustard (SM), also known as mustard gas, has been the most widely used chemical weapon. The toxicity of SM as an incapacitating agent is of much greater...

Acute and delayed sulfur mustard toxicity; novel mechanisms and future studies

Online veröffentlicht: 01. Nov. 2010

Seitenbereich: 22 - 26

DOI: https://doi.org/10.2478/v10102-010-0027-x

Schlüsselwörter
sulfur mustard, acute toxicity, delayed toxicity, melatonin, epigenetic aberrations

This content is open access.

Acute and delayed sulfur mustard toxicity; novel mechanisms and future studies

Online veröffentlicht: 01. Nov. 2010

Seitenbereich: 22 - 26

DOI: https://doi.org/10.2478/v10102-010-0027-x

Schlüsselwörtersulfur mustard, acute toxicity, delayed toxicity, melatonin, epigenetic aberrations

This content is open access.

Schlüsselwörter
sulfur mustard, acute toxicity, delayed toxicity, melatonin, epigenetic aberrations