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Int J Toxicol. 2011 Mar;30(2):197-206. doi: 10.1177/1091581810390824. Epub 2011 Feb 7.

Sodium pyruvate modulates cell death pathways in HaCaT keratinocytes exposed to half-mustard gas.

Author information

  • 1Department of Pharmacology, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37604, USA. paromov@etsu.edu

Abstract

2-Chloroethyl ethyl sulfide (CEES) or half-mustard gas, a sulfur mustard (HD) analog, is a genotoxic agent that causes oxidative stress and induces both apoptotic and necrotic cell death. Sodium pyruvate induced a necrosis-to-apoptosis shift in HaCaT cells exposed to CEES levels ≤ 1.5 mmol/L and lowered markers of DNA damage, oxidative stress, and inflammation. This study provides a rationale for the future development of multicomponent therapies for HD toxicity in the skin. We hypothesize that a combination of pyruvates with scavengers/antioxidants encapsulated in liposomes for optimal local delivery should be therapeutically beneficial against HD-induced skin injury. However, the latter suggestion should be verified in animal models exposed to HD.

PMID:
21300769
[PubMed - indexed for MEDLINE]
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