On the promoting action of tamoxifen in a model of hepatocarcinogenesis induced by p-dimethylaminoazobenzene in CF1 mice

Background and aims: Tamoxifen (TMX) has proven to be an effective palliative treatment for advanced breast cancer with low reported incidence of side effects. TMX has been demonstrated to be an initiator and/or a promoter in the rat model of hepatocarcinogenesis. To document the long-term effect of...

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Autor principal: Caballero, F.
Otros Autores: Gerez, E., Oliveri, L., Falcoff, N., Batlle, A., Vazquez, E.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2001
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Acceso en línea:Registro en Scopus
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024 7 |2 scopus  |a 2-s2.0-0034995019 
024 7 |2 cas  |a 5-Aminolevulinate Synthetase, EC 2.3.1.37; Carcinogens; Catalase, EC 1.11.1.6; Cytochrome P-450 Enzyme System, 9035-51-2; Glutathione Transferase, EC 2.5.1.18; Heme Oxygenase (Decyclizing), EC 1.14.99.3; p-Dimethylaminoazobenzene, 60-11-7; Superoxide Dismutase, EC 1.15.1.1; Tamoxifen, 10540-29-1; Thiobarbituric Acid Reactive Substances 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a IJBBF 
100 1 |a Caballero, F. 
245 1 3 |a On the promoting action of tamoxifen in a model of hepatocarcinogenesis induced by p-dimethylaminoazobenzene in CF1 mice 
260 |c 2001 
270 1 0 |m Batlle, A.Viamonte 1881 10o 'A', C1056ABA-Buenos Aires, Argentina; email: battle@mail.retina.ar 
506 |2 openaire  |e Política editorial 
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504 |a Williams, G.M., Iatropoulos, M.J., Hard, G.C., Long-term prophylactic use of tamoxifen: Is it safe? (1992) Eur. J. Cancer Prevent., 1, pp. 386-387 
504 |a Hirsimäki, P., Hirsimäki, Y., Nieminen, L., Payne, B., Tamoxifen induces hepatocellular carcinoma in rat liver: A one year study with two carcinogens (1993) Arch. Toxicol., 67, pp. 49-54 
504 |a Wogan, G., Review of the toxicology of tamoxifen (1997) Semin. Oncol., 24, pp. S187-S197 
504 |a White, I.N.H., De Matteis, F., Davies, A., Smith, L.L., Crofton-Sleigh, C., Venitt, S., Hewer, A., Phillips, D.H., Genotoxic potential of tamoxifen and analogues in female Fischer F344/n rats, DBA/2 and C57B1/6 mice and in human MCL-5 cells (1992) Carcinogenesis, 13, pp. 2197-2203 
504 |a Carthew, P., Nartin, E.A., White, I.N., De Matteis, F., Edwards, R.E., Dorman, B.M., Heydon, R.T., Smith, L.L., Tamoxifen induces short-term cumulative DNA damage and liver tumors in rats: Promotion by phenobarbital (1995) Cancer Res., 55, pp. 544-547 
504 |a Pathak, D.N., Badell, W.Y., DNA adducts formation by tamoxifen with rat and human liver microsomal activating systems (1994) Carcinogenesis, 15, pp. 529-532 
504 |a Dragan, Y., Fahey, S., Nuwaysir, E., Sattler, C., Babcock, K., Vaughan, J., McCague, R., Pitot, H., The effect of tamoxifen and two of its non-isomerizable fixed-ring analogues on multistage rat hepatocarcinogenesis (1996) Carcinogenesis, 17, pp. 585-594 
504 |a Smith, L., White, I., Chemoprevention of breast cancer by tamoxifen: Risks and opportunities (1995) Toxicol. Lett., 82, pp. 181-186 
504 |a Ghia, M., Mereto, E., Induction and promotion of gamma-glutamyltranspeptidase-positive foci in the liver of female rats treated with ethinyl estradiol, clomiphene, tamoxifen and their associations (1989) Cancer Lett., 46, pp. 195-202 
504 |a Dragan, Y.P., Fahey, S., Street, K., Vaughan, J., Jordan, V.C., Pitot, H.C., Studies of tamoxifen as a promoter of hepatocarcinogenesis in female Fischer F344 rats (1994) Breast Cancer Res. Treat., 31, pp. 11-25 
504 |a Gerez, E., Vazquez, E., Caballero, F., Polo, C., Batlle, A., Altered heme pathway regulation and drug metabolizing enzyme system in a mouse model of hepatocarcinogenesis. Effect of veronal (1997) Gen. Pharmacol., 29, pp. 569-573 
504 |a Vazquez, E., Gerez, E., Caballero, F., Polo, C., Batlle, A., Drug metabolizing enzyme system and heme pathway in hepatocarcinogenesis (1999) Cancer Biochem. Biophys., 17, pp. 25-34 
504 |a Gerez, E., Caballero, F., Vazquez, E., Polo, C., Batlle, A., Hepatic enzymatic metabolism alteration and oxidative stress during the onset of carcinogenesis: Protective role of alpha tocopherol (1998) Eur. J. Cancer Prev., 7, pp. 69-76 
504 |a Marver, H., Tschudy, D., Perlroth, M., Collins, A., δ-aminolevulinic acid synthetase. I. Studies in liver homogenates (1966) J. Biol. Chem., 241, pp. 2803-2809 
504 |a Yoshida, T., Kikuchi, G., Purification and properties of heme oxygenase from pig spleen microsomes (1978) J. Biol. Chem., 253, pp. 4224-4229 
504 |a Omura, T., Sato, R., The carbon monoxide binding pigment of liver microsomes (1964) J. Biol. Chem., 239, pp. 2370-2378 
504 |a Habig, W., Pabst, M., Jakoby, W., Glutathione S-transferases. The first enzymatic step in mercapturic acid formation (1974) J. Biol. Chem., 249, pp. 7130-7139 
504 |a Chance, B., Maehly, A., Assay of catalases and peroxidases (1955) Methods in Enzymology, 2, pp. 764-768. , S.P. Colowick, N.O. Kaplan (Eds.), Academic Press, New York 
504 |a Paoletti, F., Aldinucci, D., Mocall, A., Caparrini, A., A sensitive spectrophotometric method for the determination of superoxide dismutase activity in tissue extracts (1986) Anal. Biochem., 154, pp. 536-541 
504 |a Niehaus, W., Samuelson, B., Formation of malondialdehyde from phospholipids arachidonate during microsomal lipid peroxidation (1968) Eur. J. Biochem., 6, pp. 126-130 
504 |a Lowry, O., Rosebrough, N., Farr, A., Randall, R., Protein measurement with the Folin-phenol reagent (1954) J. Biol. Chem., 193, pp. 265-275 
504 |a Jordan, V.C., Long-term tamoxifen therapy to control or to prevent breast cancer: Laboratory concept to clinical trial (1988) Hormones, Cell Biology and Cancer: Perspectives and Potentials, pp. 105-123. , W.D. Hankins (Ed.), Alan R. Liss, New York 
504 |a Kim, D., Han, B., Ahn, B., Lee, K., Kang, J., Tsuda, H., Promotion potential of tamoxifen on hepatocarcinogenesis in female SD or F344 rats initiated with diethylnitrosamine (1996) Cancer Lett., 104, pp. 13-19 
504 |a White, I.N.H., Davies, A., Smith, L.L., Dawson, S., De Matteis, F., Induction of CYP2B1 and 3A1 and associated monooxygenase activities by tamoxifen and certain analogues in the liver of female rats and mice (1993) Biochem. Pharmacol., 45, pp. 21-30 
504 |a Nuwaysir, E.F., Daggett, D.A., Jordan, V.C., Pitot, H.C., Phase II enzyme expression in rat liver in response to the antiestrogen tamoxifen (1996) Cancer Res., 56, pp. 3704-3710 
504 |a Lim, C.K., Yuan, Z.K., Lamb, J.H., White, I.N.H., De Matteis, F., Smith, L.L., A comparative study of tamoxifen metabolism in female rat, mouse and human liver microsomes (1994) Carcinogenesis, 15, pp. 589-593 
504 |a Pigeolet, E., Carbisier, P., Houbion, A., Lambert, D., Michiels, C., Raes, M., Zachary, M., Remacle, J., Glutathione peroxidase, superoxide dismutase, and catalase inactivation by peroxides and oxygen derived free radicals (1990) Mech. Ageing Dev., 51, pp. 283-297 
504 |a Greaves, P., Goonetilleke, R., Nunn, G., Topham, J., Orton, T., Two-year carcinogenicity study of tamoxifen in Alderley Park Wistar-derived rats (1993) Cancer Res., 53, pp. 3919-3924 
504 |a Williams, G.M., Iatropoulos, M.J., Karlsson, S., Initiating activity of anti-estrogen tamoxifen but not toremifene in rat liver (1997) Carcinogenesis, 2, pp. 1111-1117 
520 3 |a Background and aims: Tamoxifen (TMX) has proven to be an effective palliative treatment for advanced breast cancer with low reported incidence of side effects. TMX has been demonstrated to be an initiator and/or a promoter in the rat model of hepatocarcinogenesis. To document the long-term effect of TMX in mice treated with p-dimethylaminoazobenzene (DAB), we have investigated the time response action of these drugs on different biochemical parameters. Methods: A group of animals was placed on dietary DAB (0.5%, w/w) during a period of 28 weeks. Control animals received a standard laboratory diet. Two other groups of non-treated and DAB-treated animals received TMX citrate (0.025%, w/w) in the diet since day 20. Results: The activities of the enzymes involved in heme synthesis and degradation as evaluated in the DAB group was not further affected by TMX. DAB and/or TMX treatment significantly increased the content of total cytochrome P450 and also the activity of glutathione S-transferase indicating liver damage. In all treated groups oxidative stress and an adaptive response of the natural defense system (catalase and superoxide dismutase) were demonstrated. Histological and morphological studies revealed liver cell hyperplasia in DAB treated group; however, only in the DAB+TMX group solid, trabecular and acinar hepatocellular carcinoma was confirmed at the end of the experimental trial. Conclusion: We have demonstrated that TMX produced changes in hepatic enzyme activities which may be relevant for the metabolism and disposition of this and/or other drugs. Because liver tumors could be initiated and promoted by several agents which need to be activated, the possible hazard of TMX should be considered. This study reports that long-term treatment with TMX enhances hepatocarcinogenesis induced by DAB. The widespread use of TMX as an anticancer agent adds to the significance of this study. © 2001 Published by Elsevier Science Ltd.  |l eng 
536 |a Detalles de la financiación: Universidad de Buenos Aires 
536 |a Detalles de la financiación: Agency for Science, Technology and Research 
536 |a Detalles de la financiación: Association for International Cancer Research, AICR 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas 
536 |a Detalles de la financiación: We are very grateful to B. Corvalan and the staff of the Department of Pathology of Dr Bernardo Houssay Hospital for valuable technical assistance during this study. A. Batlle and E. Vazquez are members of the Career of Scientific Researcher at the Argentine National Research Council (CONICET). F. Caballero and E. Gerez hold the post of Research Assistant at the CONICET. N. Falcoff is head of the Department of Pathology at the Hospital ‘Dr Bernardo Houssay’, Vicente López. This work has been supported by grants from CONICET; the University of Buenos Aires, Argentina; AICR, UK; and the Science and Technology Argentine Agency. 
593 |a Centro De Investigaciones Sobre Porfirinas Y Porfirias (CIPYP) (CONICET-FCENUBA), Ciudad Universitaria, Pabellón II, 2do piso, 1428 Buenos Aires, Argentina 
593 |a Department of Pathology, Hospital 'Dr Bernardo Houssay', Vicente López, Buenos Aires, Argentina 
593 |a Viamonte 1881 10o 'A', C1056ABA-Buenos Aires, Argentina 
690 1 0 |a CYTOCHROME P450 
690 1 0 |a HEPATOCARCINOGENESIS 
690 1 0 |a OXIDATIVE STRESS 
690 1 0 |a P-DIMETHYLAMINOAZOBENZENE 
690 1 0 |a TAMOXIFEN 
690 1 0 |a 4 DIMETHYLAMINOAZOBENZENE 
690 1 0 |a ANTINEOPLASTIC AGENT 
690 1 0 |a CATALASE 
690 1 0 |a CYTOCHROME P450 
690 1 0 |a GLUTATHIONE TRANSFERASE 
690 1 0 |a LIVER ENZYME 
690 1 0 |a SUPEROXIDE DISMUTASE 
690 1 0 |a TAMOXIFEN 
690 1 0 |a TAMOXIFEN CITRATE 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL MODEL 
690 1 0 |a ANIMAL TISSUE 
690 1 0 |a ARTICLE 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DEGRADATION 
690 1 0 |a DIET 
690 1 0 |a ENZYME ACTIVITY 
690 1 0 |a HEME SYNTHESIS 
690 1 0 |a LIVER CARCINOGENESIS 
690 1 0 |a LIVER CELL CARCINOMA 
690 1 0 |a LIVER INJURY 
690 1 0 |a LIVER TUMOR 
690 1 0 |a LONG TERM CARE 
690 1 0 |a MALE 
690 1 0 |a MOUSE 
690 1 0 |a NONHUMAN 
690 1 0 |a OXIDATIVE STRESS 
690 1 0 |a RESPONSE TIME 
690 1 0 |a 5-AMINOLEVULINATE SYNTHETASE 
690 1 0 |a ANIMALS 
690 1 0 |a BODY WEIGHT 
690 1 0 |a CARCINOGENS 
690 1 0 |a CATALASE 
690 1 0 |a CYTOCHROME P-450 ENZYME SYSTEM 
690 1 0 |a GLUTATHIONE TRANSFERASE 
690 1 0 |a HEME OXYGENASE (DECYCLIZING) 
690 1 0 |a LIVER 
690 1 0 |a LIVER NEOPLASMS, EXPERIMENTAL 
690 1 0 |a MALE 
690 1 0 |a MICE 
690 1 0 |a ORGAN SIZE 
690 1 0 |a P-DIMETHYLAMINOAZOBENZENE 
690 1 0 |a SUPEROXIDE DISMUTASE 
690 1 0 |a TAMOXIFEN 
690 1 0 |a THIOBARBITURIC ACID REACTIVE SUBSTANCES 
690 1 0 |a TIME FACTORS 
690 1 0 |a ANIMALIA 
651 4 |a LIVER HYPERPLASIA 
700 1 |a Gerez, E. 
700 1 |a Oliveri, L. 
700 1 |a Falcoff, N. 
700 1 |a Batlle, A. 
700 1 |a Vazquez, E. 
773 0 |d 2001  |g v. 33  |h pp. 681-690  |k n. 7  |p Int. J. Biochem. Cell Biol.  |x 13572725  |w (AR-BaUEN)CENRE-5218  |t International Journal of Biochemistry and Cell Biology 
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