| | Nrf3-deficient mice are not protected against acute lung and adipose tissue damages induced by butylated hydroxytolueneEdited by Laszlo Nagy Received 4 December 2009; received in revised form 12 January 2010; accepted 14 January 2010. published online 18 January 2010. Abstract We found that both wild type and Nrf3 (NF-E2-related factor 3) deficient mice are sensitive to BHT single administration exhibiting respiratory distress and considerably lose body weight following treatment. At time of sacrifice, the BHT-treated Nrf3−/− mice had lost significantly more body weight than their WT counterparts. In the lung, transcript levels of the transcription factors Nrf1, Nrf2 and Nrf3 were differentially regulated by BHT treatment. In addition, genes implicated in adipogenesis were repressed following BHT exposure in the white adipose tissue. Together, our data provide the first evidence that BHT exposure not only affects lung function but also leads to impaired adipogenesis in adipocytes. Abbreviations: ARE, antioxidant response element, BHT, butylated hydroxytoluene, Cebpb, CCAAT enhancer binding protein beta, CNC, cap ‘n’ collar, Fas, fatty acid synthase, Foxf1, forkhead box f1, Gclc, catalytic subunit of glutamate cysteine ligase, Gclm, modifier subunit of glutamate cysteine ligase, Hmox1, heme oxygenase 1, Maf, musculoaponeurotic fibrosarcoma, MARE, Maf recognition element, Nrf, NF-E2-related factor, Pparg, peroxisome proliferator-activated receptor gamma, Ptgs, prostaglandin-endoperoxide synthase, Srebp1, sterol regulatory element binding protein 1, WAT, white adipose tissue, WT, wild type a Lady Davis Institute for Medical Research, McGill University, 3755 Cote Sainte-Catherine Road, Montreal, Quebec, Canada H3T 1E2 b Department of Medicine, Division of Experimental Medicine, McGill University, Montreal, Quebec, Canada c Department of Physiology, McGill University, Montreal, Quebec, Canada d Veterinary Comparative Pathology Services, Comparative Medicine & Animal Resources Centre, McGill University, McIntyre Medical Sciences Building, 3655 Promenade Sir-William-Osler, Montreal, Quebec, Canada H3G 1Y6  Corresponding author. Address: Lady Davis Institute for Medical Research, Department of Medicine, McGill University, 3755 Cote Sainte-Catherine Road, Montreal, Quebec, Canada H3T 1E2. Fax: +1 514 340 7573.
PII: S0014-5793(10)00051-7 doi:10.1016/j.febslet.2010.01.028 © 2010 Federation of European Biochemical Societies | |
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ABSTRACT
