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Effect of oxidative stress induced by vitamin E-deficiency and/or nitrogen dioxide (NO2) inhalation on Type IV and Type I allergy responses of mice was investigated. Mice were fed a vitamin E-adequate diet (control: C group) or a vitamin E-deficient diet (‐E group). The vitamin E content in the blood of C and ‐E groups was 1.58 and 0.3 µg/ ml, respectively. Mice of the C and ‐E groups were exposed to air or air containing NO2 (5‐6 ppm) (C + NO2 and ‐E + NO2 groups) by feeding them the corresponding diets for 1‐2 week. In the sensitization with 2,4-dinitrochlorobenzene (DNCB), the degree of lymph node cell proliferation of mice of the C + NO2 group, as assessed by lymph node assay, was similar to that of mice of the C group. While the degree of cell proliferation of mice of the ‐E group was lower than that of mice of the C group, the degree of cell proliferation of mice of the ‐E + NO2 group was higher than that of mice of the C and C + NO2 groups. While the DNCB-sensitized IgE levels of mice of the C + NO2 group were similar to those of mice of the C group, the IgE levels of mice of the ‐E and ‐E + NO2 groups were higher than those of the C and C + NO2 groups. While the trimellitic anhydride (TMA)-sensitized IgE levels of mice of the ‐E group were similar to those of mice of the C group, the IgE levels of mice of the C + NO2 and ‐E + NO2 groups were much higher. These results suggest that allergen-sensitized type IV and I allergy responses of mice are enhanced by oxidative stress induced by vitamin E-deficiency and/or NO2 inhalation.

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