RESUMO
Fish oil supplements have become a popular means of increasing one's dietary intake of essential polyunsaturated fatty acids. However, there is growing concern that the levels and potential health effects of lipophilic organic contaminants such as polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) may diminish some of the health benefits associated with the daily consumption of fish oil supplements. In this study, ten over-the-counter fish oil supplements available in the United States were analysed for PCBs and PBDEs and daily exposures calculated. Based on manufacturers' recommended dosages, daily intakes of PCBs and PBDEs ranged from 5 to 686 ng day(-1) and from 1 to 13 ng day(-1), respectively. Daily consumption of fish oil supplements expose consumers to PCBs and PBDEs. However, in comparison with fish ingestion, fish supplements may decrease daily PCB exposure and provide a safer pathway for individuals seeking to maintain daily recommended levels of polyunsaturated fatty acids.
Assuntos
Suplementos Nutricionais/análise , Poluentes Ambientais/administração & dosagem , Óleos de Peixe/administração & dosagem , Óleos de Peixe/química , Éteres Difenil Halogenados/administração & dosagem , Bifenilos Policlorados/administração & dosagem , Animais , Suplementos Nutricionais/efeitos adversos , Poluentes Ambientais/química , Ácidos Graxos Essenciais/administração & dosagem , Peixes , Cromatografia Gasosa-Espectrometria de Massas , Éteres Difenil Halogenados/química , Bifenilos Policlorados/química , Reprodutibilidade dos Testes , Alimentos Marinhos/efeitos adversos , Alimentos Marinhos/análise , Estados UnidosRESUMO
Induction of cytochrome P4501A1 by 2,3,7,8-tetra-chlorodibenzo-p-dioxin (TCDD) is mediated by the Ah receptor (AhR) complex, a ligand-dependent DNA-binding transactivator. Recently a role for protein kinase C (PKC) in the induction response has been reported in which PKC or a related kinase positively modulates AhR activity. We have examined the role of PKC by determining the effect of two nonspecific PKC inhibitors, H7 and staurosporine, and one specific PKC inhibitor, calphostin c, on AhR functionality. Although no kinase activity was detectable in cytosol, under the conditions used for our assays, AhR transformation and DNA binding still occurred. Addition of relatively high concentrations of the kinase inhibitors also had no significant effect on TCDD:AhR:DRE complex formation. Thus, our results indicate that protein kinase activity does not appear to be necessary for TCDD-dependent AhR transformation and DNA binding and they imply that protein kinases must play a role in another step(s) in the AhR-dependent mechanism of P4501A1 induction.
