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Citation
Tags
HERO ID
2822029
Reference Type
Journal Article
Subtype
Review
Title
Environmental carcinogens and mutational pathways in atherosclerosis
Author(s)
Pulliero, A; Godschalk, R; Andreassi, MG; Curfs, D; Van Schooten, FJ; Izzotti, A
Year
2015
Is Peer Reviewed?
Yes
Journal
International Journal of Hygiene and Environmental Health
ISSN:
1438-4639
EISSN:
1618-131X
Publisher
ELSEVIER GMBH
Location
MUNICH
Volume
218
Issue
3
Page Numbers
293-312
Language
English
PMID
25704189
DOI
10.1016/j.ijheh.2015.01.007
Web of Science Id
WOS:000353097400002
URL
http://www.sciencedirect.com/science/article/pii/S1438463915000176
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Abstract
Atherosclerosis is associated with DNA damage in both circulating and vessel-wall cells and DNA adducts derived from exposure to environmental mutagens are abundant in atherosclerotic vessels. Environmental chemical carcinogens identified as risk factor for atherosclerosis include polycyclic aromatic hydrocarbons (benzo(a)pyrene, dimethylbenz(a)anthracene, beta-naphthoflavone, pyrene, 3-methylcolanthrene), arsenic, cadmium, 1,3-butadiene, cigarette smoke. Accordingly, polymorphisms of genes encoding for phase I/II metabolic reaction and DNA repair are risk factor for cardiovascular diseases, although their role is negligible as compared to other risk factors. The pathogenic relevance of mutation-related molecular damage in atherosclerosis has been demonstrated in experimental animal models involving the exposure to chemical mutagens. The relevance of mutation-related events in worsening atherosclerosis prognosis has been demonstrated in human clinical studies mainly as referred to mitochondrial DNA damage. Atherosclerosis is characterized by the occurrence of high level of oxidative damage in blood vessel resulting from both endogenous and exogenous sources. Mitochondrial damage is a main endogenous source of oxidative stress whose accumulation causes activation of intrinsic apoptosis through BIRC2 inhibition and cell loss contributing to plaque development and instability. Environmental physical mutagens, including ionizing radiation, are a risk factor for atherosclerosis even at the low exposure dose occurring in case of occupational exposure or the high exposure doses occurring during radiotherapy. Conversely, the role of exciting UV radiation in atherosclerosis is still uncertain. This review summarizes the experimental and clinical evidence supporting the pathogenic role of mutation-related pathway in atherosclerosis examining the underlying molecular mechanisms.
Keywords
Carcinogens; DNA damage; Atherosclerosis; Cardiovascular diseases; Polycyclic aromatic hydrocarbons; Radiation
Tags
IRIS
•
Ammonia, Oral - Problem Formulation
•
Arsenic Hazard ID
Lit Search Updates Oct 2015 to Jan 2019
ToxNet
WOS
Initial Filter
Reviews
2.5 Update 2015-2019: Title & Abstract Screening
Not relevant to PECO
•
Benzo(a)pyrene (BaP)
Cardiotox - selected for full text review (private)
Cited
NAAQS
•
ISA-PM (2019)
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