期刊
OXIDATIVE/NITROSATIVE STRESS AND DISEASE
卷 1203, 期 -, 页码 92-100出版社
WILEY-BLACKWELL
DOI: 10.1111/j.1749-6632.2010.05605.x
关键词
oxidative stress; reactive oxygen species; nitric oxide; vesicants; dermatotoxicity
资金
- National Institutes of Health [CA100994, CA093798, ES005022, ES004738, CA132624, ES017389, AR055073, AI051214, AI084137, GM034310]
- National Institutes of Health CounterACT Program through the National Institute of Arthritis and Musculoskeletal and Skin Diseases [U54AR055073]
- NATIONAL CANCER INSTITUTE [R01CA093798, R01CA132624, R01CA100994, R55CA093798] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI084137, R01AI051214, R37AI051214] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [U54AR055073] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES004738, T32ES007148, P30ES005022, F32ES017389] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM034310] Funding Source: NIH RePORTER
Sulfur mustard (SM) is a chemical weapon that targets the skin, eyes, and lung. It was first employed during World War I and it remains a significant military and civilian threat. As a bifunctional alkylating agent, SM reacts with a variety of macromolecules in target tissues including nucleic acids, proteins and lipids, as well as small molecular weight metabolites such as glutathione. By alkylating subcellular components, SM disrupts metabolism, a process that can lead to oxidative stress. Evidence for oxidative stress in tissues exposed to SM or its analogs include increased formation of reactive oxygen species, the presence of lipid peroxidation products and oxidized proteins, and increases in antioxidant enzymes such as superoxide dismutase, catalase, and glutathione-S-transferase. Inhibition of antioxidant enzymes including thioredoxin reductase by SM can also disrupt cellular redox homeostasis. Consistent with these findings, SM-induced toxicity has been shown to be reduced by antioxidants in both in vitro and in vivo models. These data indicate that drugs that target oxidative stress pathways may represent important candidates for reducing SM-induced tissue injury.
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