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Carcinogenesis hepatocarcinogenesis

Prolonged residence in the intestine or urinary bladder lumen could allow time for significant reaction with tissue components however, N-glucuronyloxy-AAF was only weakly carcinogenic at local subcutaneous sites of application (89). Enzymatic deacetylation to N-glucuronyloxy-AF has been detected in hepatic tissue but this activity in different species does not correlate with their relative susceptibility to AAF hepatocarcinogenesis (94). On the other hand, the alkaline pH-induced conversion to a reactive derivative may play an important role in urinary bladder carcinogenesis (87) by AAF and other arylamides in those species or individuals where normal urine pH is alkaline (e.g. normal rabbit urine pH is 8.5-9.0). [Pg.353]

Tanaka T, Mori Y, Morishita Y, Hara A, Ohno T, Kojinna T and Mori H. 1990. Inhibitory effect of sinigrin and indole-3-carbinol on diethylenitrosamine-induced hepatocarcinogenesis in male AC/N rats. Carcinogenesis 11 1403—1406. [Pg.49]

Sirica AE, Wilkerson CS, Wu LL, et al. 1989. Evaluation of chlordecone in a two-stage model of hepatocarcinogenesis A significant sex difference in the hepatocellular carcinoma incidence. Carcinogenesis 10(6) 1047-1054. [Pg.284]

Jensen RK, Sleight SD, Goodman JI, et al. 1982. Polybrominated biphenyls as promoters in experimental hepatocarcinogenesis in rats. Carcinogenesis 3 1183-1186. [Pg.433]

Kelly, J.D., Omer, G.A., Hendricks, J.D. Williams, D.E. (1992) Dietary hydrogen peroxide enhances hepatocarcinogenesis in trout correlation with 8-hydroxy-2 -deoxyguanosine levels in liver DNA. Carcinogenesis, 13, 1639-1642... [Pg.686]

HayashiF, Tamura H, Yamada J, et al. 1994. Characteristics of the hepatocarcinogenesis cause by dehydroepiandrosterone, a peroxisomeproliferator, in maleF-344 rats. Carcinogenesis 15(10) 2215-2219. [Pg.268]

Oganesian, A., J.D. Hendricks, C.B. Pereira, G.A. Omer, G.S. Bailey and D.E. Williams. Potency of dietary indole-3-carbinol as a promoter of aflatoxin B-l-initiated hepatocarcinogenesis results from a 9000 animal tumor study. Carcinogenesis 20 453-458, 1999. [Pg.286]

Dragan, Y. R, Campbell, H. A., Xu, X. H., and Pitot, H. C. (1997). Quantitative stereological studies of a selection protocol of hepatocarcinogenesis following initiation in neonatal male and female rats. Carcinogenesis 18(1), 149—158. [Pg.158]

Yang, Q., Ito, S., and Gonzalez, F. J. (2007). Hepatocyte-restricted constitutive activation of RRAR alpha induces hepatoproliferation but not hepatocarcinogenesis. Carcinogenesis 2, 1171-1177. [Pg.481]

LaPorta, C.A.M., and CommolU, R. (1994) Membrane and Nuclear Protein Kinase C Activation in Early Stages of Di-ethylnitrosamine-Induced Rat Hepatocarcinogenesis, Carcinogenesis 15,1734-1747. [Pg.191]

We have been interested in the effect of poly(ADP-ribosyl)ation on chemical carcinogenesis in vivo. The system used was the induction of hepatocarcinogenesis by methylazoxymethanol acetate (MAM acetate) in the small fish Medaka", Oryzias latipes. Medaka was selected as a suitable model animal for the following reasons It is easy to breed, adapts to a wide range of temperatures, is easy to sexually differentiate, has a short reproductive cycle, and is available as a pure strain. In addition, continuous administration to Medaka of the drug is possible by simply dissolving it in tank water. [Pg.480]

Pitot HC, Barsness L, Kitagawa T (1978) Stage in process of hepatocarcinogenesis in rat liver. In Slage TJ, Sivak A, Boutwell RK (eds) Mechanisms of tumor promotion and carcinogenesis. Raven Press, New York, p 433... [Pg.495]


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