Inhibition of carcinogens

WATTENBERG L (1981) Inhibition of carcinogen-induced neoplasia by sodiiun cyanate, tert-butylisocyanate and benzyl isothiocyanate administered subsequent to carcinogen exposure . Cancer Res, 41, 2991-4. [Pg.44]

WATTENBERG L w (1977) Inhibition of carcinogenic effects of polycyclic hydrocarbons by benzyl isothiocyanate and related compormds , J Nat Cancer Inst, 58 395-8. [Pg.59]

Figure 15.2 Inhibition of carcinogen activation and induction of phase II detoxification enzymes by resveratrol.

Wattenberg LW. 1972. Inhibition of carcinogenic and toxic effects of polycyclic hydrocarbons by phenolic antioxidants and ethoxyquin. J Natl Cancer Inst 48 1425-1430. [Pg.425]

Wattenberg, L.W. Inhibition of carcinogenic and Toxic Effects of Polycyclic Hydrocarbons by Phenolic Antioxidants and Ethoxyquin. J. Natl Cancer Inst, 48 1425-1430, 1972. [Pg.251]

Induction of GST activity5-6 Inhibition of carcinogenic metabolites (NNK, NDEA, DMBA, NMU)7-8-9 Alteration of gene expression through the inhibition of protein isoprenylation410 Reduced AOM-induced aberrant crypt foci12... [Pg.182]

Depletion of cellular substrates involved in activation of carcinogens can result in Inhibition of carcinogenicity (35-37). In these studies, it was shown that acetanilide decreased the liver carcinogenicity of 2-acetyl aminofluorine (2-AAF) by decreasing the formation of the ultimate carcinogenic metabolite, the sulfate ester of 2-AAF, mainly through depletion of the available sulfate as a result of sulfation of p-hydroxy acetanilide (36,37). [Pg.125]

A184. Wattenberg, L.W. Inhibition of carcinogenic effects 27A03. [Pg.1478]

Shukla Y, Singh A, Srivastava B. Inhibition of carcinogen-induced activity of gamma-glutamyl transpeptidase by certain dietary constituents in mouse skin. Biomed Environ Sci 1999 12 110-115. [Pg.165]

Inhibition of TPA-induced superoxide and hydrogen peroxide formation Inhibition of TPA-induced Epstein-Barr vims activation Induction of apoptosis and inhibition of transformation and metastasis Inhibition of carcinogen activation and DNA binding Stimulation of carcinogen detoxification Suppression of tumor cell proliferation Induction of apoptosis... [Pg.693]

Lo, W. B. and Black, H. S. Inhibition of carcinogen formation in skin 229. irradiated with ultraviolet light. Nature, 246 489-491,1973. [Pg.609]

Milo GE, Kurian P, Kirsten E, Kun E (1985) Inhibition of carcinogen induced cellular transformation of human fibroblast by drugs that interact with the poly(ADP-ribose) polymerase system. FEBS Lett 179(2) 332-336... [Pg.479]

Another response of most eukaryotic cells to carcinogen-mediated DNA strand breaks is poly(ADP-ribosyl)ation of a variety of nuclear proteins, catalyzed by poly(ADP-ribose) polymerase. We dierefore studied a possible role of poly(ADP-ribose) synthesis in carcinogen-inducible DNA amplification in a SV40 transformed Chinese hamster cell line (CO 60) which shows amplification of integrated viral sequences after carcinogen treatment (5, 7). We found that inhibition of carcinogen-stimulated poly(ADP-ribose) synthesis by 3-aminobenzamide (SAB) is correlated with an enhancement of inducible DNA amplification in CO 60 cells (13). [Pg.245]

The anti-initiation activity was demonstrated by its antioxidant and antimutagenic effects, inhibition of carcinogen bioactivation, induction of phase 11 drug-metabolizing enzymes, and the stimulation of DNA repair. [Pg.2296]

The antioxidant properties of ascorbate are often cited as the primary factor underlying associations of the vitamin with decreased cancer risk (Gershoff, 1993 Block, 1992) and mortality (Enstrom et al., 1992). However, other actions of the vitamin may also play a part, including enhanced immunocompetence and inhibition of carcinogenic nitrosamine formation. [Pg.10]

Binding/inhibition of carcinogens Antibiotic resistance (Specific risks related to host, strain characteristics, or interactions)... [Pg.270]

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