Silva, MaísaGuerra, Joyce Ferreira da CostaSampaio, Ana Flávia SantosLima, Wanderson Geraldo deSilva, Marcelo EustáquioPedrosa, Maria Lúcia2015-03-252015-03-252015SILVA, M. et al. Iron dextran increases hepatic oxidative stress and alters expression of genes related to lipid metabolism contributing to hyperlipidaemia in murine model. BioMed Research International, v. 2015, p. 1-9, 2015. Disponível em: <http://www.hindawi.com/journals/bmri/2015/272617/>. Acesso em: 20 fev. 2015.2314-6141http://www.repositorio.ufop.br/handle/123456789/4743The objective of this study was to investigate the effects of iron dextran on lipid metabolism and to determine the involvement of oxidative stress. Fischer ratswere divided into two groups: the standard group (S),whichwas fed the AIN-93Mdiet, and the standard plus iron group (SI), which was fed the same diet but also received iron dextran injections. Serum cholesterol and triacylglycerol levels were higher in the SI group than in the S group. Iron dextran was associated with decreased mRNA levels of ppar, and its downstream gene cpt1a, which is involved in lipid oxidation. Iron dextran also increased mRNA levels of apoB-100, MTP, and LFABP indicating alterations in lipid secretion. Carbonyl protein and TBARS were consistently higher in the liver of the iron-treated rats. Moreover, a significant positive correlation was found between oxidative stress products, lfabp expression, and iron stores. In addition, a negative correlation was found between ppar expression, TBARS, carbonyl protein, and iron stores. In conclusion, our results suggest that the increase observed in the transport of lipids in the bloodstream and the decreased fatty acid oxidation in rats, which was promoted by iron dextran, might be attributed to increased oxidative stress.en-USArtigo publicado em periodicoThis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Fonte: BioMed Research International <http://www.hindawi.com/journals/bmri/2015/272617/>. Acesso em: 20 fev. 2015.http://dx.doi.org/10.1155/2015/272617