ArticleJournal of cellular physiology2013
Polycyclic aromatic hydrocarbons-induced ROS accumulation enhances mutagenic potential of T-antigen from human polyomavirus JC.
Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 47 citations in OpenAlex.
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- Indoor Air Sources of Outdoor Air Pollution: Health Consequences, Policy, and Recommendations: An Official American Thoracic Society Workshop Report.Annals of the American Thoracic Society · 2024Article
- Gene-environment interactions underlying the etiology of neural tube defects.Current topics in developmental biology · 2023Article
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- A multi-omic investigation of male lower urinary tract symptoms: Potential role for JC virus.PloS one · 2021Article
- DNA-protein crosslinks from environmental exposure: Mechanisms of formation and repair.Environmental and molecular mutagenesis · 2020Review
- Tea and Its Components Prevent Cancer: A Review of the Redox-Related Mechanism.International journal of molecular sciences · 2019Review
- A bioenergetics assay for studying the effects of environmental stressors on mitochondrial function in vivo in zebrafish larvae.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2017Article
- Short-term markers of DNA damage among roofers who work with hot asphalt.Environmental health : a global access science source · 2016Article
- Elevated monocyte phosphorylated p38 in nearby employees after a chemical explosion.Scientific reports · 2016Article
- Environmental stress in the Gulf of Mexico and its potential impact on public health.Environmental research · 2016Article
- Cumulative PM(2.5) exposure and telomere length in workers exposed to welding fumes.Journal of toxicology and environmental health. Part A · 2014Article
- Recent publications by ochsner authors.Ochsner journal · 2013Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Polycyclic aromatic hydrocarbons (PAHs) are the products of incomplete combustion of organic materials, which are present in cigarette smoke, deep-fried food, and in natural crude oil. Since PAH-metabolites form DNA adducts and cause oxidative DNA damage, we asked if these environmental carcinogens could affect transforming potential of the human Polyomavirus JC oncoprotein, T-antigen (JCV T-antigen). We extracted DMSO soluble PAHs from Deepwater Horizon oil spill in the Gulf of Mexico (oil-PAHs), and detected several carcinogenic PAHs. The oil-PAHs were tested in exponentially growing cultures of normal mouse fibroblasts (R508), and in R508 stably expressing JCV T-antigen (R508/T). The oil-PAHs were cytotoxic only at relatively high doses (1:50-1:100 dilution), and at 1:500 dilution the growth and cell survival rates were practically unaffected. This non-toxic dose triggered however, a significant accumulation of reactive oxygen species (ROS), caused oxidative DNA damage and the formation of DNA double strand breaks (DSBs). Although oil-PAHs induced similar levels of DNA damage in R508 and R508/T cells, only T-antigen expressing cells demonstrated inhibition of high fidelity DNA repair by homologous recombination (HRR). In contrast, low-fidelity repair by non-homologous end joining (NHEJ) was unaffected. This potential mutagenic shift between DNA repair mechanisms was accompanied by a significant increase in clonal growth of R508/T cells chronically exposed to low doses of the oil-PAHs. Our results indicate for the first time carcinogenic synergy in which oil-PAHs trigger oxidative DNA damage and JCV T-antigen compromises DNA repair fidelity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.