Sulfur mustard induced oxidative stress and its alteration by epigallocatechin gallate

Sulfur mustard (bis(2-chloroethyl)sulfide; CAS: 505-60-2; abbreviated as HD) is a chemical warfare agent with not well understood mechanism of toxic effect. Deprivation of energy in cells and arising of oxidative stress appears during the exposure. Our experiment is based on investigation of 10 mg or 20 mg epigallocatechin gallate (EGCG) dose prophylactic effect (1 h before HD) in rats exposed to either 20 mg or 80 mg of HD. Blood mass, plasma and liver were sampled. Ferric reducing antioxidant power (FRAP), reduced glutathione, thiobarbuturic acid reactive substances (TBARSs), glutathione reductase, glutathione S-transferase and caspase 3 were assessed. Animals were sacrificed one day after exposure. We found significant deprivation of low molecular weight antioxidants due to EGCG but not due to HD. However, HD depleted reduced glutathione. EGCG has no effect to influence TBARS level. EGCG and HD up-regulated glutathione reductase and EGCG down regulated glutathione S-transferase in liver tissue. Regarding caspase, EGCG had anti apoptotic potency. We discuss potency to use EGCG to ameliorate redox balance after HD exposure. The data also appoints at difficulty in antioxidant therapy as prophylaxis to the oxidative stress related toxins exposure and ambivalent modulation of oxidative stress.