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Retinoic acid can enhance the stimulation by thyroid hormone of heme oxygenase activity in the liver of thyroidectomized rats
Institution:1. Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran;2. Department of Animal Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran;3. Department of Anatomical Sciences and Biology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran;4. Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran;1. Department of Immunology, Binzhou Medical University, Yantai, Shandong 264003, PR China;2. Medicine & Pharmacy Research Center, Binzhou Medical University, Yantai, Shandong 264003, PR China;1. Institute for Molecular Bioscience, University of Queensland, 4069, Australia;2. Edison Biotechnology Institute, Ohio University, Athens, OH 45701, USA
Abstract:The effects of retinoic acid (RA) (50 μg/100 g body wt. per day) on hepativ heme oxygenase activty, δ-aminolevulinate synthase (ALAS) activity and on cytochrome P-450 content were determined in thyroidectomized rats treated with T3 (10 μg/100 g body wt. per day) or diluent. RA, when administered for 3 days, failed to influence significantly the activity of either heme oxygenase or ALAS, however, the retinoid depleted hepatic cytochrome P-450 content by 17% (P < 0.01) and microsomal heme content by 47% (P < 0.001). T3 administration enhanced heme oxygenase activity by 72% (P < 0.001) and ALAS activity by 251% (P < 0.001) above levels in diluent treated controls and depleted cytochrome P-450 levels by 55% (P < 0.001) and heme levels by 75% (P < 0.001). When RA and T3 were administered together, the retinoid markedly enhanced the T3 stimulation of heme oxygenase activity; 173% above controls (P < 0.001), and 61% above T3 alone (P < 0.001). However, RA failed to influence the effect of T3 on ALAS activity or cytochrome P-450 depletion. The results indicate that RA can influence the levels of hepatic cytochrome P-450 and can modulate the stimulation of heme oxygenase activity by thyroid hormone in vivo.
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