By R. W. Tennant (auth.), Andrew Cockburn, Lewis Smith (eds.)

"What is a nongenotoxic carcinogen?" this query recurred via­ out the Ernst Schering study starting place Workshop on nongeno­ poisonous carcinogenesis, underlining the complexity of the subject. The readability of the view that each one cancer agents act by way of mutating DNA, beginning­ best friend encouraged by means of Bruce Ames approximately twenty years in the past, has been clouded by means of the expanding numbers of compounds which aren't genotoxic yet which however could cause melanoma. there's an pressing have to in­ crease our realizing of those compounds in order that their hazards could be evaluated realistically and judgements made up of a place of knowl­ aspect and energy, instead of in worry of the unknown. A nongenotoxic carcinogen should be outlined as a compound which reasons melanoma, yet which doesn't reason harm to DNA as its basic organic task. This unfavorable definition covers various carci­ nogens performing via quite a few mechanisms. Such chemical substances usually produce tumours basically in one organ species, and there are a number of universal destinations that are affected almost always. for instance, in male rats, sure cancer agents bind to az globulin to shape a posh which eleven accumulates within the kidney tubular cells, that is by way of necrosis and compensatory telephone proliferation prime the neoplasia. different com­ mon mechanisms contain hormonal imbalance leading to thyroid tu­ mours or peroxisome proliferation leading to liver melanoma. those and different examples are studied in a few element within the papers of this book.

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In addition PAH metabolites and other aromatic compounds which have the potential to form quinoid intermediates can induce oxidative DNA damage. As mentioned above, the cellular antioxidant defenses are bound to play a role in oxidant carcinogenesis. Epidemiological studies on serum antioxidants and diet suggest that elevated levels of vitamin E and beta-carotene reduce mortality due to cancer in the lung and colon (Menkes et al. 1986; Gey 1987). In view of the multiple stages and targets where oxidants can act in carcinogenesis, it may not be astonishing that the effect of the antioxidant defense depends on the cell type and tissue.

In order to study the effect of the major antioxidant enzymes on genome vulnerability we have constructed genetic variants of promotable mouse epidermal cells JB6 clone 41 by transfection with complementary DNA (eDNA) coding for human Cu,Zn-SOD, catalase and bovine Se-GPx. Different resistance cassettes were used for the construction of each of the three expression vectors, allowing the preparation of single- and 20 P. Amstad et al. double transfectants with increased complements of one or two enzymes.

5 How Could HPLC Underestimate 8-0HdG? 6 Artifacts in GC-MS Techniques? 6 Conclusion . . . . . . . . . . . . . . . . . . . . . . References . . . . . . . . . . . . . . . . . . . . . . . . . . ), the latter being generated by the enzyme myeloperoxidase in neutrophils (for reviews, see 32 B. Halliwell Table 1. g. g. dihydroxyfumarate, pyrogallol, adrenalin) Exposure to xanthine oxidasea plus its substrates (xanthine, hypoxanthine) Addition of tumor necrosis factor See Halliwell and Aruoma (1991).

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