DNA-damaging carcinogens

DNA-damaging carcinogens. These are genotoxic/mutagenic agents, which react chemically with DNA to cause mutations. 

DNA-damaging carcinogens Epigenetic carcinogens Progressor agents... 

Frenkel, K. (1992). Carcinogen-mediated oxidant formation and oxidative DNA damage. Pharmac. Ther. 53, 127-166. 

Oikawa, S. Hirosawa, I. Hirakawa, K. Kawanishi, S. Site specificity and mechanism of oxidative DNA damage induced by carcinogenic catechol. Carcinogenesis 2001, 22, 1239-1245. 

Luminescent bacteria also allow detection of the carcinogenic effect of ge-notoxics. A dark mutant of a Photobacterium or Vibrio strain that can revert back to luminescence at an increased rate in the presence of base-substitutes or frame-shifts agents, DNA-damaging agents, DNA synthesis inhibitors, and DNA intercalating agents can be employed [171, 172],... 

Parodi, S., S.DeFlora, M.Cavanna, and others. 1981. DNA-damaging activity in vivo and bacterial mutagenicity of sixteen hydrazine derivatives as related quantitatively to their carcinogenicity. Cancer Res. 41 1469-1482. 

From appraisal of their respective resonance stabilisation, arylnitrenium ions and alkoxynitrenium ions should form with similar facility. On account of the fact that A-acetoxy-A-acetyl arylamines 7 are penultimate carcinogens in the metabolism of aromatic amines, A-acyloxy-A-alkoxyamides 3 were designed to test their potential as DNA-damaging agents. 

To develop methods to identify individual or population susceptibility to environmental carcinogens, focusing on regulatory mechanisms for metabolism of carcinogens or repair mechanisms for carcinogen induced DNA damage between individuals or populations. 

Kada, T. (1981). The DNA damaging activity of 42 coded compounds in the Rec-assay. In Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program (de Serres F. and Ashby J., Eds.). Elsevier/North Holland, Amsterdam, pp. 175— 182. 

Looked at another way, the four major carcinogenic mechanisms are DNA damage, cell toxicity, cell proliferation and oncogene activation. Any effective program to identify those drags which have the potential to cause or increase the incidence of neoplasia in humans must effectively screen for these mechanisms (Kitchin, 1999). 

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