Influence of Vitamin E on the Mitogenic Response of Murine Lymphoid Cells

Corwin, Laurence M.; Shloss, Janet

doi:10.1093/jn/110.5.916

Cited by 100 publications

(23 citation statements)

References 18 publications

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“…Weight of draining auricular lymph nodes, lymph node cell number in the lymph nodes and 3HTdR incorporation into the cells of control mice fed a vitamin E-adequate diet were higher than those of the control mice fed a vitamin E-deficient diet (Table 1 , control). Lymph node weight, lymph node cell number and 3HTdR incorporation were increased by topical exposure to DNCB, and these values from mice fed a vitamin E-adequate diet were greater than those from mice fed a vitamin E-deficient diet ( of lymphocytes to mitogen (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). However, to our knowledge, this is the first demonstration of the effect of vitamin E on sensitization response to contact allergens.…”

Section: Discussionmentioning

confidence: 98%

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

Ikarashi¹,

Tsuchiya²,

Nakamura³

et al. 1998

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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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.

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Section: Discussionmentioning

confidence: 98%

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

Ikarashi¹,

Tsuchiya²,

Nakamura³

et al. 1998

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…Vitamin E has also been shown to cause an erythropoietic response in anemic patients (10,28) and to restore cellmediated immunity by increasing the T-cell number (8).…”

Section: Discussionmentioning

confidence: 99%

Amelioration of zidovudine-induced fetal toxicity in pregnant mice

Gogu

Beckman

Agrawal

1992

Antimicrob Agents Chemother

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The effects of zidovudine (AZT) on the fetus were investigated in pregnant mice by using parameters such as the number of fetuses, fetal size, and the fetal hepatic cell clonogenic assay. AZT caused dose-dependent toxicity to the fetus upon administration via drinking water to pregnant mice from days 1 to 13 of gestation. At the 0.5-mg/ml dose level, AZT caused a decrease in the number of fetuses to 12 from an average of 16.5 in control animals, and the fetal size (crown-rump length) was reduced from 10.5 to 8.5 mm. The CFU of the erythroid progenitor cell colonies derived from the fetal hepatic cells were decreased to 38% of that of the control, and the hematocrit dropped to 33.5 + 1.7 from a control value of 42.6 ± 2.5. Concomitant administration of erythropoietin, vitamin E, or interleukin-3 to the AZT-treated pregnant mice caused a significant reversal in the AZT-induced toxicity to the fetus and to the mother's bone marrow. The success of therapeutic intervention was demonstrated by (i) restoration of the number of fetuses to the level of untreated controls, (ii) an increase in the size of fetuses to normal values, and (iii) an increase in hematocrit to >40. The results suggest that AZT is toxic to the fetus in a dose-dependent manner and that treatment with erythropoietin, vitamin E, or interleukin-3 can ameliorate the AZT-induced fetal toxicity.Significant dose-related toxicity, primarily anemia and leukopenia associated with the administration of zidovudine (AZT), remains a limiting factor in the clinical management of AIDS (13,20). With an increasing recognition of the heterosexual spread of human immunodeficiency virus (HIV) and a high rate of reproduction reported for HIVpositive women (79% in the reproductive ages), the importance of treating pregnant women with AIDS with anti-HIV drugs is apparent. A recent prospective study of infants born to HIV-seropositive mothers has concluded that approximately one-third of them will have evidence of HIV type 1 infection or AIDS by the age of 18 months (4). Furthermore, the perinatal transmission of HIV type 1 exerts a major adverse effect on the survival of the infant (21), indicating that effective antiretroviral therapy during gestation and in the perinatal period could potentially be very useful in the management of maternal transmission of HIV (23). Although AZT has been shown to cross the placental barrier and to achieve therapeutic levels in the body fluid of the infants during the first 36 h of life (7), there are relatively few published reports which describe the toxic effects of AZT on the embryo. An overview report by Ayers (3) indicated that there is no evidence of teratogenicity in the offspring of rats or rabbits given AZT during gestation; however, an increased incidence of late fetal resorption was observed. Another report demonstrated that administration of AZT to rats on day 10 of gestation had no effect on the growth or survival of the offspring (18). (27) indicated that AZT is well tolerated by pregnant women, 3 of the 7 newborns with hem...

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“…Vitamin E is known to enhance immune responses, and to stimulate mitogenic responses of lymphocytes. [3][4][5][6] The increased IgE levels caused by vitamin E-deficiency in type I allergy responses with DNCB-sensitization may be derived from increased Th2 cell activation and the production of IL-4.…”

Section: Discussionmentioning

confidence: 99%

“…Vitamin E enhances immune responses, and stimulates mitogenic responses of lymphocytes and antibody production. [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).…”

Section: Introductionmentioning

confidence: 99%

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

Hiramoto

Kujirai

et al. 2002

JOURNAL OF HEALTH SCIENCE

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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.

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Influence of Vitamin E on the Mitogenic Response of Murine Lymphoid Cells

Cited by 100 publications

References 18 publications

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

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

Amelioration of zidovudine-induced fetal toxicity in pregnant mice

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

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