EFFECT OF VITAMIN-E ON CONTACT SENSITIZATION RESPONSES INDUCED BY 2,4-DINITROCHLOROBENZENE IN MICE

The effect of vitamin E on the contact sensitization responses induced in mice by 2,4-dinitrochlorobenzene (DNCB) was studied. Mice were fed a vitamin E-adequate or a vitamin E-deficient diet for 5 weeks. The a mounts of thiobarbituric acid-reactive substances in the spleens and d raining auricular lymph nodes of mice were decreased by dietary vitami n E. Dietary vitamin E prevented lipid peroxidation in the spleens and lymph nodes of mice. Contact sensitization develops in two phases, in duction (sensitization) and elicitation. Following sensitization to DN CB on ears, draining lymph node responses, i.e., lymph node weight, to tal lymph node cell number and in vitro lymph node cell proliferation as assessed by [H-3]methyl thymidine incorporation, were examined. The se responses, activated by DNCB, were lower in the mice fed a vitamin E-deficient diet as compared with those of the mice fed a vitamin E-ad equate diet. In the elicitation phase, lymphocytes from sensitized mic e respond to the antigen and blastogenate in vitro. The blastogenesis of spleen lymphocytes in the DNCB-sensitized mice was decreased by vit amin E deficiency, which was enhanced by exogenously adding vitamin E. It was found that vitamin E deficiency decreases the contact sensitiz ation responses to DNCB in mice, but responses were restored by exogen ous vitamin E. In conclusion, vitamin E may participate in the lymphoc yte responses to contact allergens through scavenging reactive oxygen species.