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The effects of ozone inhalation on the immunological response of selenium- and vitamin E-deprived rats
Authors:M L Eskew  W J Scheuchenzuber  R W Scholz  C C Reddy  A Zarkower
Affiliation:1. Children''s Environmental Health Initiative, Rice University, 6100 Main Street, MS-2, Houston, TX 77005, United States;2. Yale University, School of Forestry and Environmental Studies, 195 Prospect St., New Haven, CT 06511, United States;3. Rice University, Department of Statistics, 6100 Main Street, Houston, TX 77005, United States;1. Barcelona Institute for Global Health (ISGlobal), Universitat Pompeu Fabra, CIBER Epidemiología y Salud Pública, Barcelona, Parc de Salut Mar, Spain;2. King Abdullah University of Science and Technology (KAUST), Computer, Electrical and Mathematical Science and Engineering Division, Saudi Arabia;3. Basque Centre for Climate Change (BC3), Sede Building 1, 1st Floor Scientific Campus of the University of the Basque Country, 48940 Leioa, Spain;4. Manhiça Health Research Center, Manhiça, Mozambique;5. Vadu Rural Health Program, KEM Hospital Research Centre, Pune, India;1. Center for Digital Health Innovation, University of California, San Francisco, California;2. Department of Urology, University of California, San Francisco, California;3. Pulmonary, Critical Care, Allergy and Sleep Medicine Division, Department of Medicine, University of California, San Francisco, California;4. Department of Surgery, University of California, San Francisco, California;5. Endocrinology Division, Department of Medicine, University of California, San Francisco, California
Abstract:Deficiencies in vitamin E (E) or Se result in immune alterations, possibly due to reduction of antioxidant activity. Such reductions might greatly compromise the ability of the immune system to deal with additional oxidant stress, as encountered during exposure to air pollutants such as ozone (O3). To study possible interactions of these oxidative stresses on immune function, male Long-Evans hooded rats were maintained 5 weeks on torula yeast-based diets, with or without the addition of E or Se. Each dietary group was subdivided into O3-exposed and nonexposed groups. Two different regimens of O3 exposure were used: continuous (1.0 ppm, 8 hr/day for 7 days) or intermittent (2.0 ppm, 8 hr/day for 4 days, 2-4 days in ambient air followed by 1 day of exposure prior to sacrifice). Exposure to O3 in either regimen resulted in increased numbers of cells recovered by pulmonary lavage. With continuous exposure this increase was due to macrophage influx and, with intermittent exposure, due to influx of both macrophages and neutrophils. Combined deficiency of E and Se led to an enhanced ability of spleen and lung cells to mediate antibody-dependent cell-mediated cytotoxicity (ADCMC). In animals deficient in E, but not Se, O3 exposure depressed spleen cell ADCMC. Deficiencies of either E or Se also depressed lymphocyte response to mitogens. Although intermittent exposure to O3 caused no changes in mitogen response, in animals exposed continuously to O3 there was a significant enhancement of this response.
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