Hepatic DNA damage in harbour porpoises (Phocoena phocoena) stranded along the English and Welsh coastlines

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, genotoxi...

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Published in:Environmental and Molecular Mutagenesis
Main Authors: Acevedo‐Whitehouse, Karina, Cole, Kathy J., Phillips, David H., Jepson, Paul D., Deaville, Rob, Arlt, Volker M.
Format: Text
Language:English
Published: John Wiley and Sons Inc. 2018
Subjects:
Online Access:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174976/
http://www.ncbi.nlm.nih.gov/pubmed/29968392
https://doi.org/10.1002/em.22205
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spelling ftpubmed:oai:pubmedcentral.nih.gov:6174976 2023-05-15T17:35:27+02:00 Hepatic DNA damage in harbour porpoises (Phocoena phocoena) stranded along the English and Welsh coastlines Acevedo‐Whitehouse, Karina Cole, Kathy J. Phillips, David H. Jepson, Paul D. Deaville, Rob Arlt, Volker M. 2018-07-03 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174976/ http://www.ncbi.nlm.nih.gov/pubmed/29968392 https://doi.org/10.1002/em.22205 en eng John Wiley and Sons Inc. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174976/ http://www.ncbi.nlm.nih.gov/pubmed/29968392 http://dx.doi.org/10.1002/em.22205 © 2018 The Authors Environmental and Molecular Mutagenesis published by Wiley Periodicals, Inc. on behalf of Environmental Mutagen Society This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. CC-BY Research Articles Text 2018 ftpubmed https://doi.org/10.1002/em.22205 2018-10-21T00:16:28Z 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 32P‐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 108 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. ... Text North Atlantic Phocoena phocoena PubMed Central (PMC) Environmental and Molecular Mutagenesis 59 7 613 624
institution Open Polar
collection PubMed Central (PMC)
op_collection_id ftpubmed
language English
topic Research Articles
spellingShingle Research Articles
Acevedo‐Whitehouse, Karina
Cole, Kathy J.
Phillips, David H.
Jepson, Paul D.
Deaville, Rob
Arlt, Volker M.
Hepatic DNA damage in harbour porpoises (Phocoena phocoena) stranded along the English and Welsh coastlines
topic_facet Research Articles
description 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 32P‐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 108 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. ...
format Text
author Acevedo‐Whitehouse, Karina
Cole, Kathy J.
Phillips, David H.
Jepson, Paul D.
Deaville, Rob
Arlt, Volker M.
author_facet Acevedo‐Whitehouse, Karina
Cole, Kathy J.
Phillips, David H.
Jepson, Paul D.
Deaville, Rob
Arlt, Volker M.
author_sort Acevedo‐Whitehouse, Karina
title Hepatic DNA damage in harbour porpoises (Phocoena phocoena) stranded along the English and Welsh coastlines
title_short Hepatic DNA damage in harbour porpoises (Phocoena phocoena) stranded along the English and Welsh coastlines
title_full Hepatic DNA damage in harbour porpoises (Phocoena phocoena) stranded along the English and Welsh coastlines
title_fullStr Hepatic DNA damage in harbour porpoises (Phocoena phocoena) stranded along the English and Welsh coastlines
title_full_unstemmed Hepatic DNA damage in harbour porpoises (Phocoena phocoena) stranded along the English and Welsh coastlines
title_sort hepatic dna damage in harbour porpoises (phocoena phocoena) stranded along the english and welsh coastlines
publisher John Wiley and Sons Inc.
publishDate 2018
url http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174976/
http://www.ncbi.nlm.nih.gov/pubmed/29968392
https://doi.org/10.1002/em.22205
genre North Atlantic
Phocoena phocoena
genre_facet North Atlantic
Phocoena phocoena
op_relation http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174976/
http://www.ncbi.nlm.nih.gov/pubmed/29968392
http://dx.doi.org/10.1002/em.22205
op_rights © 2018 The Authors Environmental and Molecular Mutagenesis published by Wiley Periodicals, Inc. on behalf of Environmental Mutagen Society
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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