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Cited by 386

The DOI matches its Crossref record; 111 of the 111 references it cites were found in a registry or an index.

Potential genotoxicity of chronically elevated nitric oxide: A review

Open access
Liu, Rui Hai, Hotchkiss, Joseph H.·1995·Mutation Research/Reviews in Genetic Toxicology

Abstract

Several human cancers are associated with chronic bacterial, viral and parasitic infections. Nitric oxide, which is a short-lived free radical produced by many types of cells for a number of important physiological functions, is elevated in these infections. Long-term exposure to elevated NO. in cells could have potential genotoxic effects on hosts. There are at least three mechanisms by which intracellular elevated NO. could exert genotoxic affects after reacting with O2. These include formation of carcinogenic N-nitroso compounds, direct deamination of DNA bases, and oxidation of DNA after formation of peroxynitrite and/or hydroxyl radicals. One or more of these mechanisms could, theoretically, explain why chronic infection increases the risk of certain cancers.

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Crossref · 10.1016/0165-1110(95)90004-7

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Metadata

Authors
Liu, R. H., & Hotchkiss, J. H.
Venue
Mutation Research/Reviews in Genetic Toxicology
Publisher
Elsevier BV
Published
1995-06
Volume
339
Issue
2
Pages
73-89
ISSN
0165-1110 (ISSN-L)
OpenAlex
W2054794305
Cited by
386
References
111
FWCI
7.48
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Potential genotoxicity of chronically elevated nitric oxide: A review. https://app.cochat.ai/papers/10.1016/0165-1110(95)90004-7
The paper
Liu, R. H., & Hotchkiss, J. H. (1995). Potential genotoxicity of chronically elevated nitric oxide: A review. Mutation Research/Reviews in Genetic Toxicology. https://doi.org/10.1016/0165-1110(95)90004-7

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.