Vitamin E status and metabolism in adult and aged aryl hydrocarbon receptor null mice |
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| Authors: | Maret G Traber Debbie J Mustacich Laura C Sullivan Scott W Leonard Amelia Ahern-Rindell Nancy Kerkvliet |
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| Institution: | 1. Linus Pauling Institute, Oregon State University, Corvallis, OR 97331-6512, USA;2. Department of Biology, University of Portland, Portland, OR 97203, USA;3. Department of Environmental Toxicology, Oregon State University, Corvallis, OR 97331, USA;1. Department of Cancer Research, Key Laboratory of Molecular Microbiology and Technology of Ministry of Education, Institute for Molecular Biology and Biochemistry, College of Life Sciences, Nankai University, PR China;2. Department of Biochemistry, State Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Nankai University, PR China;3. Department of Radiology, West China Hospital, Sichuan University, Chengdu. PR China;1. University of Pecs, Clinical Centre, Department of Medical Genetics, Szigeti 12, H-7624 Pecs, Hungary;2. Human Genetic and Pharmacogenetic Research Group, Janos Szentagothai Research Centre, Ifjusag 20, H-7624 Pecs, Hungary;3. B.A.Z County Hospital and University Teaching Hospital, Szentpeteri Gate 72-76, H-3526 Miskolc, Hungary;4. University of Pecs, Institute of Family Medicine, Akac str. 1, H-7632 Pecs, Hungary;2. Wadsworth Center, New York State Department of Health, Albany, NY; and;4. School of Public Health, State University of New York, New York, NY |
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| Abstract: | The aryl hydrocarbon receptor (AhR) is involved in regulation of mechanisms for detoxification of xenobiotics, as well as vitamin A metabolism. Vitamin E is a fat-soluble nutrient whose metabolism is initialized via the cytochrome P450 system. Thus, AhR absence could alter hepatic regulation of α-tocopherol metabolism. To test this hypothesis, we assessed vitamin E status in adult (2-5 m) and old (21-22 m), wild-type and AhR-null mice. Plasma α-tocopherol concentrations in AhR-null mice (2.3±1.2 μmol/L, n=19) were lower than those of wild-type mice (3.2±1.2, n=17, P=.0131); those in old mice (3.2±1.2, n=20) were higher than those of adults (2.2±1.0, n=16, P=.0075). Hepatic α-tocopherol concentrations were not different between genotypes, but were nearly double in old (32±8 nmol/g, n=20) as compared with adult mice (17±2, n=16, P<.0001). Hepatic Cyp3a concentrations in AhR-null mice were greater than those in wild-type mice (P=.0011). Genotype (P=.0047), sex (P<.0001) and age (P<.0001) were significant modifiers of liver α-tocopherol metabolite (α-CEHC) concentrations. In general, Cyp3a concentrations correlated with hepatic α-tocopherol (r=0.3957, P<.05) and α-CEHC (r=0.4260, P<.05) concentrations. Since there were no significant genotype differences in the hepatic α- or γ-tocopherol concentrations, AhR-null mice did not have dramatically altered vitamin E metabolism. Since they did have higher hepatic α-CEHC concentrations, these data suggest metabolism was up-regulated in the AhR-null mice in order to maintain the hepatic tocopherol concentrations similar to those of wild-type mice. |
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