The effect of long-term supplementation of food reductones, 2,5-dimethyl-4-hydroxy-3(2H)-furanone (DMHF) (2%, w/w), detected in many foodstuffs including soy sauce, and hydroxyhydroquinone (1,2,4-benzenetriol) (HHQ) (1.2%, w/w), detected in coffee, on mouse lipid peroxidation and type IV and I allergy responses was investigated. The effect of supplementation of these reductones combined with NO(2) inhalation (5-6 ppm) was also investigated. Levels of thiobarbituric acid-reactive substances in lung were remarkably increased, and those in kidney and liver were slightly decreased by supplementation of DMHF or HHQ. The degree of 2,4-dinitrochlorobenzene (DNCB)-sensitized lymph node cell proliferation as assessed by lymph node assay was remarkably enhanced by supplementation of DMHF or HHQ. Both the DNCB-sensitized and the trimellitic anhydride-sensitized increases in IgE levels of mice were enhanced to greater extent by supplementation of DMHF or HHQ. In no cases were additive effects of NO(2) inhalation observable. Allergen-sensitized type IV and I allergy responses of mice may be enhanced by supplementation of food reductones, DMHF or HHQ.

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More than 10 kinds of heterocyclic amines (HCAs), showing mutagenic and carcinogenic potency, have been isolated from cooked fish and meat. But many researchers say that the contribution ratio of HCAs to human cancer is very low. Our purpose in this experiment was to investigate the possibility of the formation of HCAs under moderate conditions, including in vivo. A mixture of d-glucose, creatinine, and amino acid such as glycine, methionine, threonine, and proline was dissolved in phosphate-buffered solution (pH7.4) and incubated at 37 degrees C, 50 degrees C, 128 degrees C. At an appropriate time, an aliquot of the reaction solution was treated with blue cotton. HCAs were separated from the blue cotton by elution with 2% ammoniacal methanol. The eluates were submitted to the Ames test, the micronucleus test for determination of mutagenicity, and also LC-MS analysis for the detection of HCAs. Nonadsorbates to blue cotton were treated with dichloromethane and then subjected to the mutagenicity test. In the Ames test, the mutagenic activity of the reaction mixture increased with an increase of the reaction temperature. The HCA fraction from 50 degrees C incubated solution showed high frequency in the micronucleus test using HepG2 cells. The dichloromethane fractions contained other type of mutagens different from HCAs. In HCA fractions, IQ, MeIQx, 4,8-DiMeIQx, and 7,8-DiMeIQ were identified. It is said that the heating process is an essential factor in the formation of HCAs. But our experiment shows that HCAs are produced not only in the cooking process, but also in moderate conditions such as 37 degrees C and 50 degrees C.

Effect of oxidative stress induced by vitamin E-deficiency and/or nitrogen dioxide (NO 2 ) 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 NO 2 (5-6 ppm) (C + NO 2 and -E + NO 2 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 + NO 2 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 + NO 2 group was higher than that of mice of the C and C + NO 2 groups. While the DNCB-sensitized IgE levels of mice of the C + NO 2 group were similar to those of mice of the C group, the IgE levels of mice of the -E and -E + NO 2 groups were higher than those of the C and C + NO 2 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 + NO 2 and -E + NO 2 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 NO 2 inhalation.