Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.18/1764
Título: Can Estuary Sediment Contaminants Interfere with the DNA Repair Capacity of HEPG2 Cells?
Autor: Pinto, Miguel
Louro, Henriqueta
Costa, Pedro Manuel
Caeiro, Sandra
SIlva, Maria João
Palavras-chave: Genotoxicidade Ambiental
DNA Repair Capacity
Estuary Sediment Contaminants
Data: 18-Set-2013
Editora: Instituto Nacional de Saúde Doutor Ricardo Jorge, IP
Resumo: Estuarine sediments tend to act as reservoirs of pollutants, many of which are acknowledged genotoxicants and potential carcinogens for humans. In addition, many of these environmental contaminants, particularly metals, have the potential to interfere with DNA repair mechanisms. Taking an impacted estuary as a case study (the Sado, SW Portugal), previous studies showed that human hepatoma cells (HepG2) exposed to extracts of sediments collected from two areas (urban/industrial and riverine/agricultural), both contaminated by distinct mixtures of organic and inorganic toxicants, revealed differential cytotoxic and genotoxic effects, consistent with contamination indices. In this context, the present study aimed at determining whether contaminants present in sediment extracts are able to interfere with the DNA repair mechanisms of HepG2 cells. Organic and inorganic contaminants were extracted (methanol:dichloromethane) from sediment samples collected in different sites of the Sado Estuary, either heavily impacted by an urban/industrial environment (site P) or by agriculture (sites E and A); a sediment collected in a potentially “clean” site was also included (site C). The repair capacity of HepG2 cells towards ethyl methanesulfonate (EMS, 5 - 40 mM, 1h) induced DNA lesions was assessed after cells recovery in the presence of non-genotoxic concentrations of each sediment extract, during 24h and 48h, using the comet assay. Negative and solvent controls were included. Preliminary results show that at 24h and 48h after exposure, 60% and 85% of EMS-induced DNA strand breakage, respectively, was spontaneously repaired by HepG2 cells. However, exposure to extracts P and A after EMS challenge, partially inhibited DNA repair given that, relatively to the spontaneous DNA repair level, 20 and 30%, of DNA damage remained unrepaired, after 24h whereas 30 and 40% remained unrepaired after 48h. Extract E slightly interfered with HepG2 DNA repair capacity (10% unrepaired damage), independently of the period of exposure. Extract C and solvent control did not interfere with DNA damage recovery, 24 and 48h after EMS exposure. Our results suggest that extracts P and A, which display the highest concentrations of PAHs and metals, respectively, produce a clear interference with the DNA repair capacity of HepG2 cells while less or no contaminated extracts (E and C, respectively) resulted in a low or no influence on DNA repair mechanisms. These results, together with the previous observations that extracts P and A were genotoxic, raise more concern on the potential hazard of estuarine contaminants on the health of exposed populations.
URI: http://hdl.handle.net/10400.18/1764
Aparece nas colecções:DGH - Apresentações orais em encontros internacionais

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