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Carcinogens metabolism

I 97. Efarris, C. C. (1989). Interindividual variation. among humans in carcinogen metabolism, DNA adduct formation and DNA repair. Carcinogenesis 10, 1563-1566. [Pg.344]

HECHT s s (1999) Chemoprevention of cancer by isothiocyanates, modifiers of carcinogen metabolism , JNutr, 129, 768S-74S. [Pg.41]

TALALAY p and FAHEY j w (2001) Phytochemicals from cruciferous plants protect against cancer by modulating carcinogen metabolism , JNutr, 131 3027S-33S. [Pg.62]

Xie, W., Yeuh, M.F., Radominska-Pandya, A., Saini, S.P., Negishi, Y., Bottroff, B.S., Cabrera, G.Y., Tukey, R.H. and Evans, R.M. (2003) Control of steroid, heme, and carcinogen metabolism by nuclear pregnane X receptor and constitutive androstane receptor. Proceedings... [Pg.312]

Kadlubar FF. Biochemical individuality and its implications for drug and carcinogen metabolism recent insights from acetyltransferase and... [Pg.270]

Cytochrome P-U50 in carcinogen metabolism. In spite of the bewildering number of carcinogens involved the important and unifying fact is, that most of the organic carcinogens are not carcinogenic per se, but require metabolic activation in situ by cytochrome P-i 50 mediated aryl hydrocarbon hydroxylase (AHH, also known as BP hydroxylase (EC 1.lU.lit.2)). [Pg.287]

Bimbaum LS. 1987. Age-related changes in carcinogen metabolism. J Am Geriatr Soc 35 51-60. [Pg.255]

Nitration opens up another pathway to metabolic activation. Nitro-PAHs are wide-spread environmental pollutants that are mutagenic and carcinogenic. Metabolism of nitro-PAHs could occur via nitro-activation (reduction to hydroxylamine, eventually leading to nitrenes that can bind to nucleotides) and/or by ring oxidation and formation of DEs. ... [Pg.136]

Analytical Chemistry Section, Laboratory of Carcinogen Metabolism, National Cancer Institute, Bethesda, MD 20014... [Pg.91]

Petruzzelli, S., De Flora, S., Bagnasco, M., Hietanen, E., Camus, A.-M., Saracci, R., Izzotti, A., Bartsch, H. Giuntini, C. (1989) Carcinogen metabolism studies in human bronchial and lung parenchymal tissues. Am. Rev. respir. Dis., 140, 417-422... [Pg.625]

L.T., Prejean, J.D. Thompson, R.B. (1985) Benzyl acetate carcinogenicity, metabolism, and disposition in Fischer 344 rats and B6C3F, mice. Toxicology, 37, 159-170... [Pg.1263]

Yu S, Kong AN. 2007. Targeting carcinogen metabolism by dietary cancer preventive compounds. Curr Cancer Drug Targets 7 416 424. [Pg.426]

Baron, J., Kawabata, T. T., Redick, J. A., et al. Localization of Carcinogen-Metabolizing Enzymes in Human and Animal Tissues. Amsterdam Elsevier, 1983. [Pg.70]

The nature of protein in the diet also appears to alter xenobiotic metabolism. Clinton and Visek ( / and Clinton and Visek (Zi.) observed that protein alters carcinogen metabolism and that fat level in the diet alters the absorption and distribution of DMBA in the tissue. The effects of protein nutriture also are observed when 1, 2-dimethylhydrazine is included in the diet. It appears that inadequate protein in the diet causes a significant decrease in hepatic MFO activity. [Pg.15]

Figure 5. Scheme of carcinogen metabolism in mammalian target tissues. [Pg.144]

We observed a protective effect of increased dietary protein on DMBA-induced breast tumor incidence when the diets varying in protein were fed prior to carcinogen administration. We have investigated the hypothesis that dietary protein may influence carcinogenesis via effects on the mixed-function oxidase (MFO) enzyme systems involved in carcinogen metabolism. [Pg.318]

Banerjee, S., Sharma, R., Kale, R.K. and Rao, A.R. (1994) Influence of certain essential oils on carcinogen-metabolizing enzymes and acid-soluble sulfhydryls mouse liver. Nutrition and Cancer 21, 263-269. [Pg.185]

Figure 7.3. The use of immunoprecipitation to assess the relative contribution of enzymes A and B in a cellular preparation to the metabolism of a chemical carcinogen. Metabolism was decreased following immunoprecipitation with increasing concentration of antibodies to enzyme B. These results indicate that enzyme B, and not enzyme A, was responsible for the metabolism of the carcinogen. Figure 7.3. The use of immunoprecipitation to assess the relative contribution of enzymes A and B in a cellular preparation to the metabolism of a chemical carcinogen. Metabolism was decreased following immunoprecipitation with increasing concentration of antibodies to enzyme B. These results indicate that enzyme B, and not enzyme A, was responsible for the metabolism of the carcinogen.

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