Genotoxicity of 2-amino-3-methylimidazo(4, 5-f)quinoline (IQ) and related compounds in Drosophila

Gräf, Ulrich; Wild, D.; Würgler, Friedrich E.

doi:10.1093/mutage/7.2.145

Cited by 13 publications

(3 citation statements)

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“…Furthermore, the results recorded in both tables demonstrate that MMS, MMC, and HN2 are powerful genotoxins capable of inducing high frequencies of total spots per fly. Moreover, it is evident that these compounds exhibit greatly enhanced mutagenic activity in chronic treatments (48 hr) compared with acute exposure (2 or 6 hr), as previously demonstrated also by Graf et al [1992], Graf [1995], and Rodriguez-Arnaiz et al [1996].…”

Section: Negative and Positive Controlssupporting

confidence: 55%

Interference of tannic acid on the genotoxicity of mitomycin C, methylmethanesulfonate, and nitrogen mustard in somatic cells ofDrosophila melanogaster

Lehmann

Gräf

Reguly

et al. 2000

Environ. Mol. Mutagen.

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Section: Negative and Positive Controlssupporting

confidence: 55%

Interference of tannic acid on the genotoxicity of mitomycin C, methylmethanesulfonate, and nitrogen mustard in somatic cells ofDrosophila melanogaster

Lehmann

Gräf

Reguly

et al. 2000

Environ. Mol. Mutagen.

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“…Thus, nitro-IQ may be present by photoactivation in airborne particles from cigarette smoke and frying meat, and humans are likely to be exposed to nitro-IQ. Nitro-IQ exhibits mutagenicity in bacterial systems (60)(61)(62) and genotoxic activities (63,64), as well as IQ.…”

Section: Heterocyclic Aminesmentioning

confidence: 99%

Role of Oxidative DNA Damage in Dietary Carcinogenesis

Hiraku

Murata

Kawanishi

2006

Genes and Environment

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Dietary factors are implicated in approximately 35% of cancers attributed to environmental factors. Although an extremely wide variety of dietary factors are considered to contribute to carcinogenesis, its precise mechanism remains to be clariˆed. We focused on the role of oxidative DNA damage in carcinogenesis mediated by various dietary factors. We investigated the mechanism of oxidative DNA damage induced by a) amino acid metabolites, in relation to carcinogenesis caused by protein intake and amino acid imbalance, b) heterocyclic amines formed during cooking meat andˆsh, c) sugar and hyperglycemiarelated aldehydes, d) carcinogens contained in fermented foods, such as urethane, e) phytoestrogens including soy iso‰avones, f) carcinogens in edible plants, such as caŠeic acid and isothiocyanate, g) food additives, such as potassium bromate and benzoyl peroxide. These dietary factors and their metabolites induced metal-mediated oxidative damage to DNA in human cultured cells and 32 P-labeled DNA fragments obtained from human cancer-relevant genes. On the basis of our results, it is concluded that polycyclic compounds, such as heterocyclic amines, can cause oxidative DNA damage, although they appear to mainly form DNA adduct. On the other hand, monocyclic and aliphatic compounds, such as amino acid metabolites and urethane, may mainly cause oxidative DNA damage whereas they do not appear to form DNA adduct. Soy iso‰avones may cause carcinogenesis through initiation via oxidative DNA damage caused by their metabolites and promotion via cell proliferation induced by themselves. In this review, we discuss the role of oxidative DNA damage as the common mechanism of dietary carcinogenesis.

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“…Therefore, it seems likely that humans are exposed to nitro-IQ. Nitro-IQ exhibits mutagenicity in bacterial systems ( − ) and genotoxic activities ( , ), as well as IQ.…”

mentioning

confidence: 99%

Nonenzymatic Reduction of Nitro Derivative of a Heterocyclic Amine IQ by NADH and Cu(II) Leads to Oxidative DNA Damage

1999

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Nitro derivative (nitro-IQ) of a carcinogenic heterocyclic amine 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) is known to be a potent mutagen as well as IQ, and nitro-IQ is believed to be activated enzymatically by nitroreductase. We investigated nonenzymatic reduction of nitro-IQ by an endogenous reductant NADH and the ability of inducing DNA damage by nitro-IQ. Nitro-IQ caused DNA damage including 8-oxo-7,8-dihydro-2'-deoxyguanosine in the presence of NADH and Cu(II). Catalase and bathocuproine, a Cu(I)-specific chelator, inhibited the DNA damage, suggesting the involvement of H2O2 and Cu(I). Nitro-IQ induced DNA cleavage frequently at thymine and cytosine residues in the presence of NADH and Cu(II). UV-vis spectroscopic study showed that no spectral change of Nitro-IQ and NADH was observed in the absence of Cu(II), while rapid spectral change was observed in the presence of Cu(II), suggesting that Cu(II) mediated redox reaction of nitro-IQ and NADH. These results suggest that nitro-IQ can be reduced nonenzymatically by NADH in the presence of Cu(II), and the redox reaction resulted in oxidative DNA damage due to the copper-oxygen complex, derived from the reaction of Cu(I) with H2O2. We conclude that nonenzymatic reduction of nitro-IQ and resulting in oxidative DNA damage can play a role in carcinogenesis of IQ.

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Genotoxicity of 2-amino-3-methylimidazo(4, 5-f)quinoline (IQ) and related compounds in Drosophila

Cited by 13 publications

References 1 publication

Interference of tannic acid on the genotoxicity of mitomycin C, methylmethanesulfonate, and nitrogen mustard in somatic cells ofDrosophila melanogaster

Interference of tannic acid on the genotoxicity of mitomycin C, methylmethanesulfonate, and nitrogen mustard in somatic cells ofDrosophila melanogaster

Role of Oxidative DNA Damage in Dietary Carcinogenesis

Nonenzymatic Reduction of Nitro Derivative of a Heterocyclic Amine IQ by NADH and Cu(II) Leads to Oxidative DNA Damage

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