Subacute Effect of Decabromodiphenyl Ethane on Hepatotoxicity and Hepatic Enzyme Activity in Rats
Information regarding decabromodiphenyl ethane (DBDPE) effects on hepatotoxicity and metabolism is limited. In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyres...
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Veröffentlicht in: | Biomedical and environmental sciences 2014-02, Vol.27 (2), p.122-125 |
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description | Information regarding decabromodiphenyl ethane (DBDPE) effects on hepatotoxicity and metabolism is limited. In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyresorufin O-depentylase (PROD) activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase (LBD) activity. UDPGT activity increased with its increasing exposure levels, suggesting that oral DBDPE exposure induces drug-metabolizing enzymes in rats via the CAR/PXR signaling pathway. The induction of CYPs and co-regulated enzymes of phase II biotransformation may affect the homeostasis of endogenous substrates, including thyroid hormones, which may, in turn, alter glucose metabolism. |
doi_str_mv | 10.3967/bes2014.026 |
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In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyresorufin O-depentylase (PROD) activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase (LBD) activity. UDPGT activity increased with its increasing exposure levels, suggesting that oral DBDPE exposure induces drug-metabolizing enzymes in rats via the CAR/PXR signaling pathway. The induction of CYPs and co-regulated enzymes of phase II biotransformation may affect the homeostasis of endogenous substrates, including thyroid hormones, which may, in turn, alter glucose metabolism.</description><identifier>ISSN: 0895-3988</identifier><identifier>EISSN: 2214-0190</identifier><identifier>DOI: 10.3967/bes2014.026</identifier><identifier>PMID: 24625403</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Bromobenzenes - toxicity ; Chemical and Drug Induced Liver Injury - enzymology ; Chemical and Drug Induced Liver Injury - etiology ; Female ; Flame Retardants - toxicity ; Liver - drug effects ; Liver - metabolism ; Male ; Random Allocation ; Rats ; Rats, Wistar ; Toxicity Tests ; Wistar大鼠 ; 亚急性 ; 十溴二苯乙烷 ; 甲状腺激素 ; 肝损伤 ; 药物代谢酶 ; 葡萄糖代谢 ; 酶活性</subject><ispartof>Biomedical and environmental sciences, 2014-02, Vol.27 (2), p.122-125</ispartof><rights>2014 The Editorial Board of Biomedical and Environmental Sciences</rights><rights>Copyright © 2014 The Editorial Board of Biomedical and Environmental Sciences. Published by China CDC. All rights reserved.</rights><rights>Copyright © Wanfang Data Co. Ltd. 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In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyresorufin O-depentylase (PROD) activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase (LBD) activity. UDPGT activity increased with its increasing exposure levels, suggesting that oral DBDPE exposure induces drug-metabolizing enzymes in rats via the CAR/PXR signaling pathway. The induction of CYPs and co-regulated enzymes of phase II biotransformation may affect the homeostasis of endogenous substrates, including thyroid hormones, which may, in turn, alter glucose metabolism.</description><subject>Animals</subject><subject>Bromobenzenes - toxicity</subject><subject>Chemical and Drug Induced Liver Injury - enzymology</subject><subject>Chemical and Drug Induced Liver Injury - etiology</subject><subject>Female</subject><subject>Flame Retardants - toxicity</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Toxicity Tests</subject><subject>Wistar大鼠</subject><subject>亚急性</subject><subject>十溴二苯乙烷</subject><subject>甲状腺激素</subject><subject>肝损伤</subject><subject>药物代谢酶</subject><subject>葡萄糖代谢</subject><subject>酶活性</subject><issn>0895-3988</issn><issn>2214-0190</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kUlPHDEQha0oKAwkp9wjR8qBS5Py0ouPiEwACSlSlrNlu6sZo2l7aLshk18fo545WSp_9erVK0I-MrgUqmm_WkwcmLwE3rwhK86ZrIApeEtW0Km6EqrrTslZSo8AkinZvSOnXDa8liBWxPyarXFzRroeBnSZxoF-Q2fsFMfY-90Gw35L13ljAtIY6C3uTI45_vXO5z01oV9K3tF1-LcfkV657J9f_3ygP01O78nJYLYJPxzec_Ln-_r39W11_-Pm7vrqvnKC8VxhI4prhyBxcHUrGuDG9hbYwEttMAw7Zhj0WFsURloBbStq27JOCtvUjTgnXxbdFxMGEx70Y5ynUCbqQ0DAAdqCXSzYbopPM6asR58cbrdlwTgnzeoirARXsqCfDuhsR-z1bvKjmfb6mF4B6gXAstezx0kn5zE47P1UstR99JqBfr3S0YQuVyp9n5c-t4nh4ckXs0dtqQqgVCf-A244jUU</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>SUN, Ru Bao</creator><creator>XI, Zhu Ge</creator><creator>ZHANG, Hua Shan</creator><creator>ZHANG, Wei</creator><general>Elsevier B.V</general><general>Beijing Institute of Disease Control and Prevention, Beijing 100071, China%Tianjin Institute of Health and Environmental Medicine, Tianjin 300050, China</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope></search><sort><creationdate>20140201</creationdate><title>Subacute Effect of Decabromodiphenyl Ethane on Hepatotoxicity and Hepatic Enzyme Activity in Rats</title><author>SUN, Ru Bao ; 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In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyresorufin O-depentylase (PROD) activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase (LBD) activity. UDPGT activity increased with its increasing exposure levels, suggesting that oral DBDPE exposure induces drug-metabolizing enzymes in rats via the CAR/PXR signaling pathway. The induction of CYPs and co-regulated enzymes of phase II biotransformation may affect the homeostasis of endogenous substrates, including thyroid hormones, which may, in turn, alter glucose metabolism.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>24625403</pmid><doi>10.3967/bes2014.026</doi><tpages>4</tpages></addata></record> |
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subjects | Animals Bromobenzenes - toxicity Chemical and Drug Induced Liver Injury - enzymology Chemical and Drug Induced Liver Injury - etiology Female Flame Retardants - toxicity Liver - drug effects Liver - metabolism Male Random Allocation Rats Rats, Wistar Toxicity Tests Wistar大鼠 亚急性 十溴二苯乙烷 甲状腺激素 肝损伤 药物代谢酶 葡萄糖代谢 酶活性 |
title | Subacute Effect of Decabromodiphenyl Ethane on Hepatotoxicity and Hepatic Enzyme Activity in Rats |
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