Short-term markers of DNA damage among roofers who work with hot asphalt

Serdar, Berrin; Brindley, Stephen; Dooley, Greg; Volckens, John; Juaréz-Colunga, Elizabeth; Gan, Ryan W.

doi:10.1186/s12940-016-0182-4

Cited by 7 publications

(4 citation statements)

References 80 publications

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“…[ 172 , 173 ]). LC-MS/MS is the main methodology for the majority of these matrices, emphasizing the strength of this approach, although ELISA has been used for serum [ 125 , 174 , 175 ], saliva [ [176] , [177] , [178] , [179] ], sputum [ 180 ], follicular fluid [ 169 , 170 ], and urine [ [181] , [182] , [183] , [184] ] (for others, see the ELISA section below).…”

Section: Measurement Of Oxidised Nucleic Acid Products In Extracellular Biological Matricesmentioning

confidence: 99%

Biomarkers of nucleic acid oxidation – A summary state-of-the-art

Chao

Evans

et al. 2021

Redox Biology

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Oxidatively generated damage to DNA has been implicated in the pathogenesis of a wide variety of diseases. Increasingly, interest is also focusing upon the effects of damage to the other nucleic acids, RNA and the (2′-deoxy-)ribonucleotide pools, and evidence is growing that these too may have an important role in disease. LC-MS/MS has the ability to provide absolute quantification of specific biomarkers, such as 8-oxo-7,8-dihydro-2′-deoxyGuo (8-oxodG), in both nuclear and mitochondrial DNA, and 8-oxoGuo in RNA. However, significant quantities of tissue are needed, limiting its use in human biomonitoring studies. In contrast, the comet assay requires much less material, and as little as 5 μL of blood may be used, offering a minimally invasive means of assessing oxidative stress in vivo , but this is restricted to nuclear DNA damage only. Urine is an ideal matrix in which to non-invasively study nucleic acid-derived biomarkers of oxidative stress, and considerable progress has been made towards robustly validating these measurements, not least through the efforts of the European Standards Committee on Urinary (DNA) Lesion Analysis. For urine, LC-MS/MS is considered the gold standard approach, and although there have been improvements to the ELISA methodology, this is largely limited to 8-oxodG. Emerging DNA adductomics approaches, which either comprehensively assess the totality of adducts in DNA, or map DNA damage across the nuclear and mitochondrial genomes, offer the potential to considerably advance our understanding of the mechanistic role of oxidatively damaged nucleic acids in disease.

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Section: Measurement Of Oxidised Nucleic Acid Products In Extracellular Biological Matricesmentioning

confidence: 99%

Biomarkers of nucleic acid oxidation – A summary state-of-the-art

Chao

Evans

et al. 2021

Redox Biology

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“…12 As an internationally recognized biomarker of DNA oxidative damage, 8-OHdG is stabilized in the body; it is not affected by the diet or cellular renewal and it can be induced by various xenobiotics. 13-15 Several studies have also suggested that 8-OHdG is linked to many kinds of diseases, from tumors, cardiovascular disease to diabetes. 16-18 However, to the best of our knowledge, few previous studies have evaluated the impact of IR on 8-OHdG levels.…”

Section: Introductionmentioning

confidence: 99%

Serum 8-Hydroxy-2′-Deoxyguanosine Level as a Potential Biomarker of Oxidative DNA Damage Induced by Ionizing Radiation in Human Peripheral Blood

Gao

Wang

et al. 2019

Dose-Response

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In this study, the effect of ionizing radiation on 8-hydroxy-2′-deoxyguanosine (8-OHdG) in human peripheral blood was investigated. Blood samples were collected from 230 radiation workers and 8 patients who underwent radiotherapy for population study. Blood samples from 2 healthy individuals were irradiated with different X-ray doses for in vitro experiment, and levels of 8-OHdG in serum and cell culture supernatants were assessed by enzyme-linked immunosorbent assay. Observations demonstrated the positive relationships between serum 8-OHdG level and radiation dose and working period were observed, and serum 8-OHdG levels were higher among interventional radiation workers than among other hospital radiation workers. In addition, 8-OHdG yields in supernatants increased, peaked at 3 Gy of radiation dose, and then decreased with further increases in radiation; the dose–response curve obtained fitted a polynomial function. By contrast, a similar trend was not found in radiotherapy patients. The present study suggests that 8-OHdG may be a useful biomarker reflecting oxidative damage among workers occupationally exposed to low-dose radiation.

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“…B[ a ]P is a known group 1 carcinogen according to the IARC [9,10], while other genotoxic HMW PAHs are primarily classified as group 2B, “possibly carcinogenic to humans”. However, low molecular weight (LMW; 2–4 rings) PAHs are more abundant than HMW PAHs, such as B[ a ]P, in primary and SHS smoke from cigarettes and marijuana (e.g., fluoranthene), in air pollution as components of particulate matter, as well as potential occupational hazards for those workers in industries such as coal, coke, and steel [1,2,3,9,11,12,13,14,15,16,17]. For example, in SHS, the level of 2–4 ring LMW PAHs is ~20 times that of the HMW PAHs [2] and in the Kentucky 1R1 reference cigarette smoke condensates, the methylated anthracenes (LMW PAHs) are 62 times higher than B[ a ]P and benzo( e )pyrene [11].…”

Section: Introductionmentioning

confidence: 99%

Dysregulation of Gap Junction Function and Cytokine Production in Response to Non-Genotoxic Polycyclic Aromatic Hydrocarbons in an In Vitro Lung Cell Model

Romo

Velmurugan

Upham

et al. 2019

Cancers

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Polycyclic aromatic hydrocarbons (PAHs), prevalent contaminants in our environment, in many occupations, and in first and second-hand smoke, pose significant adverse health effects. Most research focused on the genotoxic high molecular weight PAHs (e.g., benzo[a]pyrene), however, the nongenotoxic low molecular weight (LMW) PAHs are emerging as potential co-carcinogens and tumor promoters known to dysregulate gap junctional intercellular communication (GJIC), activate mitogen activated protein kinase pathways, and induce the release of inflammatory mediators. We hypothesize that inflammatory mediators resulting from LMW PAH exposure in mouse lung epithelial cell lines are involved in the dysregulation of GJIC. We used mouse lung epithelial cell lines and an alveolar macrophage cell line in the presence of a binary PAH mixture (1:1 ratio of fluoranthene and 1-methylanthracene; PAH mixture). Parthenolide, a pan-inflammation inhibitor, reversed the PAH-induced inhibition of GJIC, the decreased CX43 expression, and the induction of KC and TNF. To further determine the direct role of a cytokine in regulating GJIC, recombinant TNF (rTNF) was used to inhibit GJIC and this response was further enhanced in the presence of the PAH mixture. Collectively, these findings support a role for inflammation in regulating GJIC and the potential to target these early stage cancer pathways for therapeutics.

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Short-term markers of DNA damage among roofers who work with hot asphalt

Cited by 7 publications

References 80 publications

Biomarkers of nucleic acid oxidation – A summary state-of-the-art

Biomarkers of nucleic acid oxidation – A summary state-of-the-art

Serum 8-Hydroxy-2′-Deoxyguanosine Level as a Potential Biomarker of Oxidative DNA Damage Induced by Ionizing Radiation in Human Peripheral Blood

Dysregulation of Gap Junction Function and Cytokine Production in Response to Non-Genotoxic Polycyclic Aromatic Hydrocarbons in an In Vitro Lung Cell Model

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