ArticleGenes and environment : the official journal of the Japanese Environmental Mutagen Society2024
Rosmarinic acid, a natural polyphenol, has a potential pro-oxidant risk via NADH-mediated oxidative DNA damage.
Article in Genes and environment : the official journal of the Japanese Environmental Mutagen Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- Molecular Mechanisms of Basil (Molecules (Basel, Switzerland) · 2026Article
- Novel Strategy for Cancer Therapy Proposal Based on Effects and Mechanisms of Targeting Cuproptosis by Polyphenols-A Narrative Review.Nutrients · 2026Review
- The Chinese herb component salvianolic acid B induces copper-mediated reactive oxygen species generation and oxidative DNA damage.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025Article
- Liposomal Delivery of a BiotechnologicalAntioxidants (Basel, Switzerland) · 2025Article
- Impact of glycolysis enzymes and metabolites in regulating DNA damage repair in tumorigenesis and therapy.Cell communication and signaling : CCS · 2025Review
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7 authors.
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Abstract
backgroundRosmarinic acid (RA) has a wide range of beneficial effects on human health. On the other hand, RA has been reported to induce metal-mediated reactive oxygen species (ROS) generation and DNA damage. However, its mechanism remains unknown. In this study, to clarify the underlying mechanism, we analyzed metal-mediated DNA damage in isolated DNA treated with RA and its analog isorinic acid.
resultsRA plus Cu(II), but not Fe(III), significantly increased 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) formation, an indicator of oxidative DNA damage, in calf thymus DNA. Furthermore, a comparison of the 8-oxodG formation induced by RA and its analog isorinic acid suggested that the catechol groups in RA could be associated with their abilities to form 8-oxodG. Interestingly, the 8-oxodG formation induced by RA and isorinic acid plus Cu(II) was markedly enhanced by the addition of NADH, an endogenous reductant. To elucidate the mechanism of RA plus Cu(II)-induced oxidative DNA damage, we examined DNA damage in
conclusionsIn this study, physiologically relevant concentrations of RA effectively induced oxidative DNA damage in isolated DNA through redox cycle reactions with copper and NADH.
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