Hepatic DNA damage in harbour porpoises (Phocoena phocoena) stranded along the English and Welsh coastlines. (3rd July 2018)

• Record Type: Journal Article
• Authors: Acevedo‐Whitehouse, Karina; Cole, Kathy J.; Phillips, David H.; Jepson, Paul D.; Deaville, Rob; Arlt, Volker M.
• Is Part Of: Environmental and molecular mutagenesis. Volume 59:Number 7(2018)
• Page Start: 613
• Page End: 624
• Publication Date: 2018-07-03
• Subjects: DNA damage -- harbour porpoise -- genotoxicity -- persistent organic pollutants (POPs) -- polychlorinated biphenyls (PCBs) -- polycyclic aromatic hydrocarbons (PAHs) -- 32P‐postlabeling; Mutagenesis -- Periodicals; Molecular genetics -- Periodicals; Mutagenèse -- Périodiques; Mutagenèse chimique -- Périodiques; Mutation -- Périodiques; Maladies de l'environnement -- Périodiques; Génétique moléculaire -- Périodiques; 576.542
• DOI: 10.1002/em.22205
• Languages: English
• ISSNs: 0893-6692

Abstract

Abstract : One level at which persistent organic pollutants (POPs) and polycyclic aromatic hydrocarbons PAHs) can exert damage is by causing DNA strand‐breaks or nucleotide base modifications, which, if unrepaired, can lead to embryonic mutations, abnormal development and cancer. In marine ecosystems, genotoxicity is expected to be particularly strong in long‐lived apex predators due to pollutant bioaccumulation. We conducted 32 P‐postlabeling analyses optimized for the detection and quantification of aromatic/hydrophobic DNA adducts in the livers of 40 sexually‐mature North Atlantic harbour porpoises ( Phocoena phocoena ) stranded along the English and Welsh coastlines. We examined hepatic tissue to search for inflammatory and preneoplastic lesions and examine their association with adduct levels. Adducts were found in all porpoises (mean: 17.56 ± 11.95 per 10 8 nucleotides), and were higher than levels reported for marine vertebrates from polluted sites. The pollutants causing the induced DNA adducts could not be further characterized. Hepatic DNA damage did not correlate with levels of blubber POP concentrations (including total polychlorinated biphenyl [PCBs], dichlorodiphenyltrichloroethane [DDT] and dieldrin); PAH concentrations were not available for the present study. However, DNA damage predicted occurrence of inflammatory and preneoplastic lesions. Further, our data showed a reduction in hepatic DNA adduct levels with age in the 40 animals examined while POP concentrations, particularly PCBs, increased with age. Using a different dataset of 145 mature male harbour porpoises confirmed that higher contaminant levels (total PCBs, DDT and dieldrin) are found in older animals. The reduction in hepatic DNA adduct levels in older animals was in accordance with other studies which show that suppression of hepatic CYP1A enzyme activity at high PCB concentrations might impact on CYP1A‐mediated DNA adduct formation of PAHs which are ubiquitous environmental pollutants and readily metabolized by CYP1A to species binding to DNA. In summary, our study shows that pollutant‐induced DNA damage is prevalent in harbour porpoises from UK waters and may lead to detectable sub‐lethal hepatic damage. Environ. Mol. Mutagen. 59:613–624, 2018. © 2018 The Authors Environmental and Molecular Mutagenesis published by Wiley Periodicals, Inc. on behalf of Environmental Mutagen Society