Drug metabolizing enzyme system and heme pathway in hepatocarcinogenesis

Chemically induced and spontaneous liver tumors share some metabolic alterations. The decline in hemoprotein levels during hepatocarcinogenesis may result from a diminution of the intracellular heme pool. To elucidate if the onset of the pre-initiation stage alters the natural regulation mechanism o...

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Autor principal: Vazquez, E.
Otros Autores: Gerez, E., Caballero, F., Polo, C., Batlle, A.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 1999
Acceso en línea:Registro en Scopus
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LEADER 09831caa a22014417a 4500
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024 7 |2 scopus  |a 2-s2.0-0032826563 
024 7 |2 cas  |a 5-Aminolevulinate Synthetase, EC 2.3.1.37; Allylisopropylacetamide, 299-78-5; Carcinogens; Cytochrome P-450 Enzyme System, 9035-51-2; Enzyme Inhibitors; Glucuronidase, EC 3.2.1.31; Glutathione Transferase, EC 2.5.1.18; Heme Oxygenase (Decyclizing), EC 1.14.99.3; Heme, 14875-96-8; Hemeproteins; p-Dimethylaminoazobenzene, 60-11-7; Prodrugs; Sulfatases, EC 3.1.6.-; Tryptophan Oxygenase, EC 1.13.11.11 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a CABCD 
100 1 |a Vazquez, E. 
245 1 0 |a Drug metabolizing enzyme system and heme pathway in hepatocarcinogenesis 
260 |c 1999 
270 1 0 |m Batlle, A.Viamonte 1881 10. ''A', 1056 - Buenos Aires, Argentina; email: cipyp@alad.fcen.uba.ar 
506 |2 openaire  |e Política editorial 
504 |a Becker, F., Stout, D., A constitutive deficiency in the monooxygenase system of spontaneous mouse liver tumors (1984) Carcinogenesis, 5, pp. 785-788 
504 |a Chance, B., Maehly, A., Assay of catalases and peroxidases (1955) Methods Enzymol., 2, pp. 764-768. , E. Chance and A. Maebly (Eds.), Academic Press, New York 
504 |a Degawa, M., Chemical carcinogenesis and cytochrome P 450 Carcinogenic aromatic amine-induced P450 and hepatocarcinogenic susceptibility to the aromatic amine in the rodent (1995) Yakugaku Zasshi. J. Pharmac Soc Japan, 115, pp. 1-14 
504 |a El-Mouelhi, M., Didolkar, M., Elias, E., Guenguerich, F., Kauffman, F., Hepatic drug metabolizing enzymes in primary and secondary tumors of human liver (1987) Cancer Res., 47, pp. 460-4667 
504 |a Farber, E., Cellular biochemistry of the stepwise development of cancer with chemicals: G.H.A. Clowes Memorial Lectures (1984) Cancer Res., 44, pp. 5463-5474 
504 |a Farber, E., Clonal adaptation as an important phase of hepatocarcinogenesis (1991) Cancer Biochem. Biophys., 12, pp. 157-165 
504 |a Farber, E., Parker, S., Gruenstein, M., The resistance of putative premalignant liver cell populations, hyperplastic nodules, to the acute cytotoxic effects of some hepatocarcinogens (1976) Cancer Res., 36, pp. 3879-3887 
504 |a Habib, S., Srikanth, N., Scappaticci, F., Faletto, M., Maccubbin, A., Farber, E., Ghoshal, A., Gurtoo, H., Altered expression of cytochrome P450 mRNA during chemical-induced hepatocarcinogenesis and following patial hepatectomy (1994) Toxicol. Appl. Pharmacol., 124, pp. 139-148 
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 Kanduc, D., Aresta, A., Farber, E., Hypermethylation of replicating hepatic DNA following N- Methyl-N-nitrosourea administration (1994) Int. J. Cancer, 58, pp. 436-439 
504 |a Knox, W., L-Tryptophan 2,3-dioxy genase (trytophan pyrrolase) (rat liver) (1970) Methods Enzymol., 17, pp. 415-417 
504 |a Koo, P., Nagai, M., Farber, E., Multiple sites of control of glutathione S-transferase PI-1 in rat liver (1994) J. Biol. Chem., 269, pp. 14601-14606 
504 |a Lowry, O., Rosebrough, N., Farr, A., Randall, R., Protein measurement with the Folin-phenol reagent (1951) J. Biol. Chem., 193, pp. 265-275 
504 |a Marver, H., Tsehudy, D., Perlroth, M., Collins, A., δ-aminolevulinic acid synthetase. I. Studies in liver homogenates (1966) J. Biol. Chem., 241, pp. 2803-2809 
504 |a Miller, J., Brief history of chemical carcinogenesis (1994) Cancer Lett., 83, pp. 9-14 
504 |a Omura, T., Sato, R., The carbon monoxide binding pigment of liver microsomes (1964) J. Biol Chem., 239, pp. 2370-2378 
504 |a Ozawa, S., Abu-Zeid, M., Murayama, N., Yamazoe, Y., Kato, R., Decreases in metabolic activating capacities of arylamines in livers bearing hyperplastic nodules: Association with the selective changes in hepatic P-450 isoenzymes (1990) Jpn. J. Cancer Res., 81, pp. 247-252 
504 |a Parke, D., The cytochromes P 450 and mechanisms of chemical carcinogenesis (1994) Environ. H1th. Perspect., 102, pp. 852-853 
504 |a Polo, C., Vazquez, E., Caballero, F., Gerez, E., Batlle, A., Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation (1992) Comp. Biochem. Physiol., 103 B, pp. 251-256 
504 |a Sakai, T., Klopman, G., Rosenkranz, H., Structural basis for the induction of preneoplastic glutathione S-transferase positive pool by hepatocarcinogens (1994) Teratogenesis, Carcinogenesis and Mutagenesis, 14, pp. 219-237 
504 |a Stout, D., The role of transferrin in heme transport (1994) Biochem. Biophys Res. Commun., 189, pp. 765-770 
504 |a Stout, D., Becker, F., Heme enzyme pattern in genetically and chemically induced mouse liver tumors (1986) Cancer Res., 46, pp. 2756-2759 
504 |a Stout, D., Becker, F., Heme enzyme pattern in rat liver nodules and tumors (1987) Cancer Res., 47, pp. 963-966 
504 |a Sultatos, L., Vessell, E., Enhanced drug metabolizing capacity within liver adjacent to human and rat liver tumors (1980) Proc. Natn. Acad. Sci. USA, 77, pp. 600-603 
504 |a Yoshida, T., Kikuchi, G., Purification and properties of heme oxygenase from pig spleen microsomes (1978) J. Biol. Chem., 253, pp. 4224-4229 
520 3 |a Chemically induced and spontaneous liver tumors share some metabolic alterations. The decline in hemoprotein levels during hepatocarcinogenesis may result from a diminution of the intracellular heme pool. To elucidate if the onset of the pre-initiation stage alters the natural regulation mechanism of heme pathway, animals were fed with p-dimethylaminoazobenzene (DAB) and treated or not with 2-allylisopropylacetamide (AIA). The induction of 6-Aminolevulinic acid synthase (ALA-S) activity and the diminution in microsomal heme oxygenase (MHO) did not change when DAB fed animals were treated with AIA. Cytochrome P-450 (P-450) levels and glutathione S-transferase activity were increased in all the groups tested. Tryptophan pyrrolase, sulphatase and β-glucuronidase activities were altered in DAB fed animals but AIA treatment did not produce any effect. Changes in drug metabolizing enzymes in livers of DAB fed animals could be the result of a primary deregulation of heme metabolism. These results give additional support to our hypothesis about a mechanism for the onset of hepatocarcinogenesis.  |l eng 
593 |a Ctro. Invest. Porfirinas y Porfirias, Ciudad Universitaria, Pabellón II, (1428) Buenos Aires, Argentina 
593 |a Viamonte 1881 10o, A 1056 - Buenos Aires, Argentina 
690 1 0 |a Δ-AMINOLEVULINIC ACID SYNTHASE 
690 1 0 |a 2-ALLYLISOPROPYL-ACETAMIDE 
690 1 0 |a CYTOCHROME P-450 
690 1 0 |a GLUTHATIONE S-TRANSFERASE 
690 1 0 |a HEPATOCARCINOGENESIS 
690 1 0 |a MICROSOMAL HEME OXYGENASE 
690 1 0 |a 4 DIMETHYLAMINOAZOBENZENE 
690 1 0 |a 5 AMINOLEVULINATE SYNTHASE 
690 1 0 |a ALLYLISOPROPYLACETAMIDE 
690 1 0 |a BETA GLUCURONIDASE 
690 1 0 |a CARCINOGEN 
690 1 0 |a CYTOCHROME P450 
690 1 0 |a ENZYME INHIBITOR 
690 1 0 |a GLUTATHIONE TRANSFERASE 
690 1 0 |a HEME 
690 1 0 |a HEME OXYGENASE 
690 1 0 |a HEMOPROTEIN 
690 1 0 |a PRODRUG 
690 1 0 |a SULFATASE 
690 1 0 |a TRYPTOPHAN 2,3 DIOXYGENASE 
690 1 0 |a ANIMAL 
690 1 0 |a ARTICLE 
690 1 0 |a BIOLOGICAL MODEL 
690 1 0 |a BIOTRANSFORMATION 
690 1 0 |a CELL TRANSFORMATION 
690 1 0 |a CHEMICALLY INDUCED DISORDER 
690 1 0 |a COMPARATIVE STUDY 
690 1 0 |a DRUG ANTAGONISM 
690 1 0 |a DRUG EFFECT 
690 1 0 |a DRUG RESISTANCE 
690 1 0 |a ENZYME INDUCTION 
690 1 0 |a ENZYMOLOGY 
690 1 0 |a LIVER MICROSOME 
690 1 0 |a LIVER TUMOR 
690 1 0 |a MALE 
690 1 0 |a METABOLISM 
690 1 0 |a MOUSE 
690 1 0 |a OXIDATION REDUCTION REACTION 
690 1 0 |a PHYSIOLOGY 
690 1 0 |a PRECANCER 
690 1 0 |a 5-AMINOLEVULINATE SYNTHETASE 
690 1 0 |a ALLYLISOPROPYLACETAMIDE 
690 1 0 |a ANIMALS 
690 1 0 |a BIOTRANSFORMATION 
690 1 0 |a CARCINOGENS 
690 1 0 |a CELL TRANSFORMATION, NEOPLASTIC 
690 1 0 |a CYTOCHROME P-450 ENZYME SYSTEM 
690 1 0 |a DRUG RESISTANCE 
690 1 0 |a ENZYME INDUCTION 
690 1 0 |a ENZYME INHIBITORS 
690 1 0 |a GLUCURONIDASE 
690 1 0 |a GLUTATHIONE TRANSFERASE 
690 1 0 |a HEME 
690 1 0 |a HEME OXYGENASE (DECYCLIZING) 
690 1 0 |a HEMEPROTEINS 
690 1 0 |a LIVER NEOPLASMS, EXPERIMENTAL 
690 1 0 |a MALE 
690 1 0 |a MICE 
690 1 0 |a MICROSOMES, LIVER 
690 1 0 |a MODELS, BIOLOGICAL 
690 1 0 |a OXIDATION-REDUCTION 
690 1 0 |a P-DIMETHYLAMINOAZOBENZENE 
690 1 0 |a PRECANCEROUS CONDITIONS 
690 1 0 |a PRODRUGS 
690 1 0 |a SULFATASES 
690 1 0 |a TRYPTOPHAN OXYGENASE 
700 1 |a Gerez, E. 
700 1 |a Caballero, F. 
700 1 |a Polo, C. 
700 1 |a Batlle, A. 
773 0 |d 1999  |g v. 17  |h pp. 25-34  |k n. 1-2  |p Cancer Biochem. Biophys.  |x 03057232  |t Cancer Biochemistry Biophysics 
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856 4 0 |u https://hdl.handle.net/20.500.12110/paper_03057232_v17_n1-2_p25_Vazquez  |y Handle 
856 4 0 |u https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03057232_v17_n1-2_p25_Vazquez  |y Registro en la Biblioteca Digital 
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