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 amounts of thiobarbituric acid-reactive substances in the spleens and draining auricular lymph nodes of mice were decreased by dietary vitamin E. Dietary vitamin E prevented lipid peroxidation in the spleens and lymph nodes of mice. Contact sensitization develops in two phases, induction (sensitization) and elicitation. Following sensitization to DNCB on ears, draining lymph node responses, i.e., lymph node weight, total lymph node cell number and in vitro lymph node cell proliferation as assessed by [3H]methyl thymidine incorporation, were examined. These 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-adequate diet. In the elicitation phase, lymphocytes from sensitized mice respond to the antigen and blastogenate in vitro. The blastogenesis of spleen lymphocytes in the DNCB-sensitized mice was decreased by vitamin E deficiency, which was enhanced by exogenously adding vitamin E. It was found that vitamin E deficiency decreases the contact sensitization responses to DNCB in mice, but responses were restored by exogenous vitamin E. In conclusion, vitamin E may participate in the lymphocyte responses to contact allergens through scavenging reactive oxygen species.