Effect of Vitamin E on Contact Sensitization Responses Induced by 2,4-Dinitrochlorobenzene in Mice.

Abstract

SummaryThe 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.

Effects of Vitamin E-Deficiency and/or Nitrogen Dioxide Inhalation on Allergen-Sensitized Type IV and Type I Allergy Responses of Mice.

“…There were no differences in weight or LNC number between unsensitized mice of C and C + NO 2 groups, or among DNCB-sensitized mice of C, -E, C + NO 2 and -E + NO 2 groups ( Table 1). As has been shown previously, 7,14) the degree of cell proliferation of mice of the C group was increased by DNCB-sensitization. The DNCB-sensitized increase in cell proliferation was not affected by NO 2 inhalation (C + NO 2 group) (Fig.…”

“…2. As has been shown in the previous papers, 7,14) the lymph node weight and total LNC number of the C group was increased by DNCB-sensitization (Table 1). There were no differences in weight or LNC number between unsensitized mice of C and C + NO 2 groups, or among DNCB-sensitized mice of C, -E, C + NO 2 and -E + NO 2 groups ( Table 1).…”

“…2). It is interesting to note that although the degree of DNCB-sensitized cell proliferation of mice of the -E group was lower than that of mice of the C group, 7) that of mice of the -E + NO 2 group was higher than those of mice of the -E group (Fig. 2).…”

“…13) In the present study, inhalation of NO 2 to mice, even in the vitamin E-deficient state, caused no remarkable increase in the degree of lipid peroxidation in the lung. Nevertheless, previous studies 7) have shown that the levels of TBARS in the spleen and lymph nodes of mice fed a vitamin Edeficient diet showed a remarkable increase in comparison to those of mice fed a vitamin E-adequate diet.…”

“…[3][4][5][6] Our previous studies have shown that vitamin E-deficiency in mice brings about decreased contact sensitization responses to 2,4-dinitrochlorobenzene (DNCB). 7) On the other hand, nitrogen dioxide (NO 2 ) is a free radical toxin usually present in polluted urban and room air (0.02-0.2 ppm), and in fresh smoke or cigarrette smoke (upto 100 ppm). It has been shown that long-term inhalation of a low level of NO 2 causes oxidative damage, especially to lung tissue.…”