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Hepatocarcinogenesis

PPAR Xenochemical Induction of CYP4A Enzymes and Role in Rodent Hepatocarcinogenesis... [Pg.892]

Persistent activation of PPARa can induce the development of hepatocellular carcinoma in susceptible rodent species by a nongenotoxic mechanism, i.e., one that does not involve direct DNA damage by peroxisome proliferator chemicals or their metabolites. This hepatocarcinogenic response is abolished in mice deficient in PPARa, underscoring the central role of PPARa, as opposed to that of two other mammalian PPAR forms (PPARy and PPAR5), in peroxisome proliferator chemical-induced hepatocarcinogenesis. Other toxic responses, such as kidney and testicular toxicities caused by exposure to certain phthalate... [Pg.892]

Ohnishi H, Asamoto M, Tujimura K, Hokaiwado N, Takahashi S, Ogawa K, et al. Inhibition of cell proliferation by nobiletin, a dietary phytochemical, associated with apoptosis and characteristic gene expression, but lack of effect on early rat hepatocarcinogenesis in vivo. Cancer Sci 2004 95 936-42. [Pg.164]

PITOT H c and dragan y p (1994) The multistage nature of chemically induced hepatocarcinogenesis in the rat . Drug Metab Rev, 26, 209-20. [Pg.42]

In their review some years ago, Reddy and Rao (1986) cited several lines of evidence for peroxisome-proliferation-mediated oxidative stress being associated with hepatocarcinogenesis. They mentioned the sustained increase in hydrogen peroxide production, the detectable increased levels of hydrogen peroxide in the livers of treated animals, increased lipid peroxidation associated with treatment and marked inhibition of hepatocarcinogenesis by antioxidant compounds. However, definitive studies remain to be carried out. [Pg.240]

N-Glucuronyloxy arylamides do not appear to be important in hepatocarcinogenesis as their increased metabolic formation does not result in increased hepatic macromolecular binding (4,25). [Pg.351]

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]

Breinholt V, Hendricks J, Pereira C, Arbogast D and Bailey G. 1995. Dietary chlorophyllin is a potent inhibitor of aflatoxin Bi hepatocarcinogenesis in rainbow trout. Cancer Res 55(l) 57-62. [Pg.38]

Sugie S, Okumura A, Tanaka T and Mori H. 1993. Inhibitory effects of benzylisothiocyanate and ben-zylthiocyanate on diethylnitrosamine-induced hepatocarcinogenesis in rats. Jpn J Cancer Res 84 865— 870. [Pg.49]

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]

Moreno FS, S-Wu T, Naves MM, Silveira ER, Oloris SC, Costa MA, Dagli ML and Ong TP. 2002. Inhibitory effects of beta-carotene and vitamin A during progression phase of hepatocarcinogenesis involve inhibition of cell proliferation but not alterations in DNA methylation. Nutr Cancer 44 80-... [Pg.217]

Sampaio ARD, Chagas CEA, Ong TP and Moreno FS. 2007. Vitamin A and 3-carotene inhibitory effect during 1,2-dimethylhydrazine induced hepatocarcinogenesis potentiated by 5-azacytidine. Food Chem... [Pg.219]

A number of early in vitro studies demonstrated a considerable role of free radicals in liver injury (see, for example, Proceedings of International Meeting on Free Radicals in Liver Injury [341]). Later on, it was shown that chronic inflammation in the liver-induced oxidative DNA damage stimulated chronic active hepatitis and increased the risk of hepatocarcinogenesis [342,343]. Farinati et al. [344] showed that 8-OHdG content increased in circulating leukocytes of patients with chronic hepatitis C virus (HCV) infection. DNA oxidative damage is supposedly an early event of HCV-related hepatitis. The formation of isoprostanes in the liver of carbon tetrachloride-treated rats can be suppressed by the administration of vitamin E [345],... [Pg.938]

Important studies were performed by Trush and coworkers [42], who showed the advantages of applying lucigenin-amplified CL for the measurement of superoxide production by mitochondria in unstimulated monocytes and macrophages as well as by isolated mitochondria [43,44]. Later on, these authors have shown that mitochondrial superoxide production measured by lucigenin-amplified CL increased in the liver of rats treated with the promoter of hepatocarcinogenesis ethinyl estradiol [45], in liver from obese mice [46], and in children with Down syndrome [47]. [Pg.966]

Donohoe, R.M., Q. Zhang, L.K. Siddens, J.D. Hendricks, and L.R. Curtis. 1998. Modulation of 7,12-dime-thylbenz[a] anthracene disposition and hepatocarcinogenesis by dieldrin and chlordecone in rainbow trout. Jour. Toxicol. Environ. Health 54A 227-242. [Pg.1398]

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]

Eischer AN, Herrera B, Mikula M, Proell V, Fuchs E, Gotzmarm J etaJ (2005). Integration of Ras snbeffector signaling in TGF- beta mediated late stage hepatocarcinogenesis. [Pg.133]

Rossmanith W, Schulte-Hermann R (2001). Biology of transforming growth factor beta in hepatocarcinogenesis. MicroscRes Tech 52 430 436. [Pg.134]

Guyonnet D, Berges R, Siess MH, Pinnert ME, Chagnon MC, Suschetet M, Le Bon AM. (2004) Post-initiation modulating effects of allyl sulfides in rat hepatocarcinogenesis. Food Chem Toxicol 42 1479-1485. [Pg.301]

Dragiani TA, Manenti G, Porta GD. 1986. Enhancing effects of carbon tetrachloride in mouse hepatocarcinogenesis. Cancer Lett 31 171-179. [Pg.158]

Zalatnai A, Sarosi I, Rot A, et al. 1991. Inhibitory and promoting effects of carbon tetrachloride-induced liver cirrhosis on the diethyinitrosamine hepatocarcinogenesis in rats. Cancer Lett 57 67- 73. [Pg.190]

Ashby, J., Brady, A., Elcombe, C.R., Elliott, B.M., Ishmael, J., Odum, J., Tugwood, J.D., Kettle, S. Purchase, I.F. (1994) Mechanistically-based human hazard assessment of peroxisome proliferator-induced hepatocarcinogenesis. Hum. exp. Toxicol., 13 (Suppl 2), S1-S117... [Pg.37]

Rodent peroxisome proliferators exercise their pleiotropic effects due to activation of PPARa. This process is essential for liver hypertrophy and hyperplasia and eventual hepatocarcinogenesis in response to peroxisome proliferators. [Pg.167]

S. Purchase, IF. (1994) Mechanistically-based human hazard assessment of peroxisome proliferator-induced hepatocarcinogenesis. Hum. exp. Toxicol., 13 (Suppl. 2), S1-S117... [Pg.189]

Pitot, H.C., Barsness, L., Goldsworthy, T., and Kitagawa, T. (1978). Biochemical characterization of stages of hepatocarcinogenesis after a single dose of diethylnitrosamine, Nature 271,456. [Pg.151]

The tumor initiating potential of PBBs is not well characterized. Numbers of GGT-altered foci were significantly increased in partially hepatectomized rats that were administered a single 1-10 mg/kg oral dose of 3,3, 4,4 -tetrabromobiphenyl followed by phenobarbital in the diet for 180 days (Dixon et al. 1988), indicating that PBBs may have initiating activity in hepatocarcinogenesis. Tlie potential for liver tumor initiation by PBBs appears to be weak compared to tlieir potent promoting activity (Buchmann et al. 1991 Dixon etal. 1988 Jensen et al. 1984). [Pg.179]

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

Sleight S. 1985. Effects of PCBs and related compounds on hepatocarcinogenesis in rats and mice. Environ Health Perspect 60 35-39. [Pg.452]

Research has shown clearly that PPARa is necessary for hepatocarcinogenesis in mice. Thus, the PPARa-agonist drug Wy-14643 causes a 100% incidence of liver tumors in wild-type mice, yet PPARa-null mice are resistant. This has been confirmed using the drug bezafibrate. [Pg.306]

However, the role proliferation of the peroxisomes in the hepatocarcinogenesis may be coincidental rather than causal, as extent of the proliferation does not correlate well with the carcinogenicity. [Pg.306]


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