ArticleChemical research in toxicology2014
Covalent adduct formation between the antihypertensive drug hydralazine and abasic sites in double- and single-stranded DNA.
Article in Chemical research in toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
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
7 citing papers in PubMed, 20 citations in OpenAlex.
- Impact ofBiomolecules · 2026Article
- Advancing Covalent Ligand and Drug Discovery beyond Cysteine.Chemical reviews · 2025Review
- Anthracyclines React with Apurinic/Apyrimidinic Sites in DNA.ACS chemical biology · 2023Article
- Article
- Preparation and Purification of Oligodeoxynucleotide Duplexes Containing a Site-Specific, Reduced, Chemically Stable Covalent Interstrand Cross-Link Between a Guanine Residue and an Abasic Site.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Small Molecule Inhibitors of 8-Oxoguanine DNA Glycosylase-1 (OGG1).ACS chemical biology · 2015Article
- Detection of oxidative stress-induced carbonylation in live mammalian cells.Free radical biology & medicine · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hydralazine (4) is an antihypertensive agent that displays both mutagenic and epigenetic properties. Here, gel electrophoretic, mass spectroscopic, and chemical kinetics methods were used to provide evidence that medicinally relevant concentrations of 4 rapidly form covalent adducts with abasic sites in double- and single-stranded DNA under physiological conditions. These findings raise the intriguing possibility that the genotoxic properties of this clinically used drug arise via reactions with an endogenous DNA lesion rather than with the canonical structure of DNA.
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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.