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Sci Total Environ. 2014 Apr 15;478:25-35. doi: 10.1016/j.scitotenv.2014.01.084. Epub 2014 Feb 12.

Determining oxidative and non-oxidative genotoxic effects driven by estuarine sediment contaminants on a human hepatoma cell line.

Author information

  • 1Departamento de Genética Humana, Instituto Nacional de Saúde Dr. Ricardo Jorge, I.P., Av. Padre Cruz, 1649-016 Lisboa, Portugal.
  • 2Departamento de Genética Humana, Instituto Nacional de Saúde Dr. Ricardo Jorge, I.P., Av. Padre Cruz, 1649-016 Lisboa, Portugal; IMAR - Instituto do Mar, Departamento de Ciências e Engenharia do Ambiente, Faculdade de Ciências e Tecnologia da Universidade Nova de Lisboa, 2829-516 Caparica, Portugal. Electronic address: pmcosta@fct.unl.pt.
  • 3IMAR - Instituto do Mar, Departamento de Ciências e Engenharia do Ambiente, Faculdade de Ciências e Tecnologia da Universidade Nova de Lisboa, 2829-516 Caparica, Portugal.
  • 4IMAR - Instituto do Mar, Departamento de Ciências e Engenharia do Ambiente, Faculdade de Ciências e Tecnologia da Universidade Nova de Lisboa, 2829-516 Caparica, Portugal; Departamento de Ciências e Tecnologia, Universidade Aberta, Rua da Escola Politécnica, 141, 1269-001 Lisboa, Portugal; CENSE - Centre for Environmental and Sustainability Research, Departamento de Ciências e Engenharia do Ambiente, Faculdade de Ciências e Tecnologia da Universidade Nova de Lisboa, 2829-516 Caparica, Portugal.

Abstract

Estuarine sediments may be reservoirs of hydrophilic and hydrophobic pollutants, many of which are acknowledged genotoxicants, pro-mutagens and even potential carcinogens for humans. Still, studies aiming at narrowing the gap between ecological and human health risk of sediment-bound contaminant mixtures are scarce. Taking an impacted estuary as a case study (the Sado, SW Portugal), HepG2 (human hepatoma) cells were exposed in vitro for 48 h to extracts of sediments collected from two areas (urban/industrial and Triverine/agricultural), both contaminated by distinct mixtures of organic and inorganic toxicants, among which are found priority mutagens such as benzo[a]pyrene. Comparatively to a control test, extracts of sediments from both impacted areas produced deleterious effects in a dose-response manner. However, sediment extracts from the industrial area caused lower replication index plus higher cytotoxicity and genotoxicity (concerning total DNA strand breakage and clastogenesis), with emphasis on micronucleus induction. On the other hand, extracts from the rural area induced the highest oxidative damage to DNA, as revealed by the FPG (formamidopyrimidine-DNA glycosylase) enzyme in the Comet assay. Although the estuary, on its whole, has been classified as moderately contaminated, the results suggest that the sediments from the industrial area are significantly genotoxic and, furthermore, elicit permanent chromosome damage, thus potentially being more mutagenic than those from the rural area. The results are consistent with contamination by pro-mutagens like polycyclic aromatic hydrocarbons (PAHs), potentiated by metals. The sediments from the agriculture-influenced area likely owe their genotoxic effects to metals and other toxicants, probably pesticides and fertilizers, and able to induce reactive oxygen species without the formation of DNA strand breakage. The findings suggest that the mixtures of contaminants present in the assayed sediments are genotoxic to HepG2 cells, ultimately providing a useful approach to hazard identification and an effective line-of-evidence in the environmental monitoring of anthropogenically-impacted coastal ecosystems.

Copyright © 2014 Elsevier B.V. All rights reserved.

KEYWORDS:

DNA damage; HepG2; Micronuclei; Oxidative stress; Sediment contamination

PMID:
24530582
[PubMed - indexed for MEDLINE]
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