ArticleProceedings of the National Academy of Sciences of the United States of America2015
Metabolic fate of endogenous molecular damage: Urinary glutathione conjugates of DNA-derived base propenals as markers of inflammation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
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- Genetically Predicted 1400 Blood Metabolites in Relation to Risk of Prostate Cancer: A Mendelian Randomization Study.Aging medicine (Milton (N.S.W)) · 2025Article
- Nucleic acid adductomics - The next generation of adductomics towards assessing environmental health risks.The Science of the total environment · 2023Article
- Biomimetic mimicry of formaldehyde-induced DNA-protein crosslinks in the confined space of a metal-organic framework.Chemical science · 2022Article
- Measurement of deaminated cytosine adducts in DNA using a novel hybrid thymine DNA glycosylase.The Journal of biological chemistry · 2022Article
- Urinary DNA adductomics - A novel approach for exposomics.Environment international · 2018Article
- Liquid Chromatography-Tandem Mass Spectrometry for the Quantification of Tobacco-Specific Nitrosamine-Induced DNA Adducts in Mammalian Cells.Analytical chemistry · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Although mechanistically linked to disease, cellular molecules damaged by endogenous processes have not emerged as significant biomarkers of inflammation and disease risk, due in part to poor understanding of their pharmacokinetic fate from tissue to excretion. Here, we use systematic metabolite profiling to define the fate of a common DNA oxidation product, base propenals, to discover such a biomarker. Based on known chemical reactivity and metabolism in liver cell extracts, 15 candidate metabolites were identified for liquid chromatography-coupled tandem mass spectrometry (LC-MS/MS) quantification in urine and bile of rats treated with thymine propenal (Tp). Analysis of urine revealed three metabolites (6% of Tp dose): thymine propenoate and two mercapturate derivatives of glutathione conjugates. Bile contained an additional four metabolites (22% of Tp dose): cysteinylglycine and cysteine derivatives of glutathione adducts. A bis-mercapturate was observed in urine of untreated rats and increased approximately three- to fourfold following CCl4-induced oxidative stress or treatment with the DNA-cleaving antitumor agent, bleomycin. Systematic metabolite profiling thus provides evidence for a metabolized DNA damage product as a candidate biomarker of inflammation and oxidative stress in humans.
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Registered trials
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