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

Victor Paromov, Marianne Brannon, Sudha Kumari, Mallikarjun Samala, Min Qui, Milton Smith, William L Stone

Index: Int. J. Toxicol. 30(2) , 197-206, (2011)

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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.