Evidence map›Paper›PMID 39853239›Full record

ArticleJournal of occupational health2025

Oxidative and nitrative DNA damage induced by industrial chemicals in relation to carcinogenesis.

Yusuke Hiraku

Abstract read
In one paragraph

Article in Journal of occupational health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Yusuke HirakuDepartment of Environmental Health, University of Fukui School of Medical Science, Eiheiji, Fukui, Japan.ORCID 0000-0002-4351-1498

Funding

Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology and the Ministry of Health, Labour and Welfare of Japan
6 · The paper itself

Abstract

objectivesMany chemicals have been used for industrial purposes, and some of them are carcinogenic to humans. However, the molecular mechanisms of their carcinogenetic effects have not been well understood. Reactive oxygen species are generated from industrial chemicals and contribute to carcinogenesis. Particles and fibers are accumulated in respiratory systems by inhalation exposure and cause chronic inflammation. Under inflammatory conditions, reactive nitrogen species are generated from inflammatory and epithelial cells. These species cause oxidative and nitrative DNA damage, leading to carcinogenesis. We carried out experiments on DNA damage induced by various industrial chemicals and investigated their molecular mechanisms.

methodsWe examined oxidative DNA damage induced by industrial chemicals using DNA fragments derived from human cancer-relevant genes by polyacrylamide gel electrophoresis. Using immunohistochemistry and immunocytochemistry we also examined the formation of 8-nitroguanine (8-nitroG), a DNA lesion formed under inflammatory conditions, in lung tissues and cultured cells exposed to industrial chemicals.

resultsBenzene and o-toluidine metabolites caused oxidative damage to DNA fragments in the presence of Cu(II). H2O2 and Cu(I) were generated during oxidation of these chemicals and involved in DNA damage. 8-NitroG formation was observed in lung tissues of asbestos-exposed mice and humans. Carbon nanomaterials and indium compounds induced 8-nitroG formation in human lung epithelial cells via the release of damage-associated molecular patterns from exposed cells.

conclusionsVarious industrial chemicals are considered to induce carcinogenesis by causing oxidative and nitrative DNA damage. These findings provide an insight into risk assessment of industrial chemicals and prevention of carcinogenesis in workplaces.

Indexed as

CarcinogenesisDNA DamageOxidative StressAnimalsAsbestosBenzeneCarcinogensGuanineHumansHydrogen PeroxideLungMaleMiceOccupational ExposureOxidation-ReductionReactive Nitrogen Species8-nitroguanineAsbestosBenzeneCarcinogensGuanineHydrogen PeroxideReactive Nitrogen SpeciesReactive Oxygen SpeciescancerDNA damageindustrial chemicalsinflammationnitric oxidereactive oxygen species

Identifiers

PMID39853239
PMCPMC12491942

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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.