ArticleJapanese journal of cancer research : Gann2001
Oxidative DNA damage induced by an N-hydroxy metabolite of carcinogenic 4-dimethylaminoazobenzene.
Article in Japanese journal of cancer research : Gann, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 34 citations in OpenAlex.
- Unsaponifiable fraction of black Vitis vinifera seed oil attenuates liver cancer progression by targeting apoptosis and key tumor-associated genes: In vitro, in vivo, and in silico studies.Scientific reports · 2026Article
- Amelioration of carcinogen-induced toxicity in mice by administration of a potentized homeopathic drug, natrum sulphuricum 200.Evidence-based complementary and alternative medicine : eCAM · 2009Article
- Protective potentials of a potentized homeopathic drug, Lycopodium-30, in ameliorating azo dye induced hepatocarcinogenesis in mice.Molecular and cellular biochemistry · 2006Article
- Identification of 100 KDa protein in sera of mice-treated with Cu(II) complex with superoxide dismutase-mimetic activity.Journal of physiology and biochemistry · 2003Article
- Oxidative DNA damage induced by a metabolite of 2-naphthylamine, a smoking-related bladder carcinogen.Japanese journal of cancer research : Gann · 2002Article
- Effect of a homeopathic drug, Chelidonium, in amelioration of p-DAB induced hepatocarcinogenesis in mice.BMC complementary and alternative medicine · 2002Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Formation of adducts has been considered to be a major causal factor of DNA damage by carcinogenic aminoazo dyes. We investigated whether a metabolite of hepatocarcinogenic 4-dimethylaminoazobenzene (DAB) can cause oxidative DNA damage or not, using (32)P-5'-end-labeled DNA fragments. The DAB metabolite N-hydroxy-4-aminoazobenzene (N-OH-AAB) was found to cause Cu(II)-mediated DNA damage, including 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) formation. When an endogenous reductant, beta-nicotinamide adenine dinucleotide (NADH) was added, the DNA damage was greatly enhanced. Very low concentrations of N-OH-AAB could induce DNA damage via redox reactions. Catalase and a Cu(I)-specific chelator inhibited the DNA damage, suggesting the involvement of H2O2 and Cu(I). A typical.OH scavenger did not inhibit the DNA damage. The main reactive species are probably DNA-copper-hydroperoxo complexes. We conclude that oxidative DNA damage may play an important role in the carcinogenic processes of DAB, in addition to DNA adduct formation.
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