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Methylcholanthrene-induced

Recently, the mechanism of 6-nitro-BaP ring hydroxylation has been elucidated by using 3-deutero-6-nitro-BaP (144). When incubated with 3-methylcholanthrene-induced rat liver microsomes, this deuterated analogue yielded the same metabolite profile previously observed with 6-nitro-BaP. Spectroscopic analysis of 3-hydroxy-6-nitro-BaP and 6-nitro-BaP-3,9-hydroquinone indicated that 30% of the deuterium label had migrated to carbon 2, presumably via an NIH shift. Therefore, it appears that 6-nitro-BaP-2,3-oxide is a common intermediate for these two metabolites. [Pg.390]

Bock KW, Schirmer G, Green MD, et al. 1988. Properties of 3-methylcholanthrene-inducible phenol UDP-glucuronosyltransferase from rat liver. Biochem Pharmacol 37 1439-1443. [Pg.204]

Kouri RE, Ratrie H, Whitmire CE. 1974. Genetic control of susceptibility to 3-methylcholanthrene-induced lung subcutaneous sarcomas. J Cancer 13 714-720. [Pg.644]

Nebert. Isolation and characterization of a cloned DNA sequence associated with the murine Ah locus and a 3-methylcholanthrene-induced form of cytochrome P-450. Proc. Natl. Acad. Sci. U.S.A. 78 800-804, 1981. [Pg.278]

Hussain, S.P. and Rao, A.R. (1991) Chemopreventive action of mace (Myristica fragrans Houtt) on methylcholanthrene-induced carcinogenesis in the uterine cervix in mice. Cancer Letters 56(3), 231-234. [Pg.186]

Knockout systems ethylnitrosourea induced uterine tumors in p53 knockout mice. susceptible to methylcholanthrene-induced tumorigenesis. [113] well studied. Can be created for most cytokines or effector cells. May provide strong proof of concept. genes. Compensatory effects may mask deficit. All or nothing effect may overestimate hazard. [Pg.614]

Huang DY, Ohnishi T, Jiang H, Furukawa A, Ichikawa Y. 1999. Inhibition by retinoids of benzo(A)pyrene metabolism catalyzed by 3-methylcholanthrene-induced rat cytochrome P-450 1A1. Metabolism 48 689-92... [Pg.331]

Aloctin A is a glycoprotein obtained from A. aborescens Miller. Aloctin A administered to six mice at a dose of 10 mg/kg/d intraperitoneally for 5 d inhibited growth of methylcholanthrene-induced fibrosarcoma in four of the mice vs zero of ten untreated mice. These results were attributed to aloctin A s immunomodulatory effect, not cytotoxicity (Imanishi et al., 1981). [Pg.329]

Imanishi K, Ishiguro T, Saito H, Suzuki I. Pharmacological studies of plant lectin, Aloctin A. I. Growth inhibition of mouse methylcholanthrene-induced fibrosarcoma (Meth A) in ascites form by Aloctin A. Experientia 1981 37 1186-7. [Pg.336]

Masuda Y, Yasoshima M. 1988. Loss of 3-methylcholanthrene-inducible form of cytochrome P-450 in liver microsomes following administration of carbon disulfide in C57BL/6 Cr mice. Biochem Pharmacol 37 2363-2371. [Pg.202]

Yasoshima M, Masuda Y. 1988. Effects of carbon disulfide on liver microsomal cytochrome p-450 in phenobarbitol and 3-methylcholanthrene-induced animals. Jpn J Pharmacol 46 ... [Pg.222]

Scuderi P, Rosse C. 1981b. The role of bone marrow cells in the growth inhibition of trasplanted methylcholanthrene-induced sarcoma (MCA). XIII(l) 747-751. [Pg.385]

Luukkanen L, Elovaara E, Lautala P, et al. 1997. Characterization of 1-hydroxypyrene as a novel marker substrate of 3-methylcholanthrene-inducible phenol UDP-glucutonosyltransferase(s). Pharmacol Toxicol 80 152-158. [Pg.334]

Ebel, S. Liedtke, R. Missler, B. [Quantitative determination of nitrofurantoin in body fluids by direct injection HPLC]. Arch.Pharm.(Weinheim)., 1980, 313, 95-96 Jonen, H.G. Oesch, F. Platt, K.L. 4-Hydroxylation of nitrofurantoin in the rat. A 3-methylcholanthrene-inducible pathway of a relatively nontoxic compound. Drug Metab.Dispos., 1980, 8, 446-451... [Pg.972]

Methylcholanthrene- induced Adenovirus type 12-induced 1x10 10x3 Tumor occurence 83 - 33 % 79 - 40 % ... [Pg.130]

Comparison of the metabolic profiles of benzo(a)pyrene obtained from primary cell cultures and subcellular fractions derived from normal and methylcholanthrene-induced rat liver. Cancer Letters 5 81-89. [Pg.83]

The rate of chromate reduction using NADH as a cofactor did not vary with the source of microsomes. The same kinetic parameters were found with control, phenobar-bital-induced and 3-methylcholanthrene-induced microsomes. Therefore there was no correlation of rate of chromate reduction with the activity of NADH-Cytochrome P-450 reductase in the microsomes which was 1.25 times greater in the control set than in either the phenobarbital- or 3-methylcholanthrene-induced microsomes. The cytochrome bs content of the microsomes, however, did not vary ( 5%) with the source of microsomes. [Pg.119]

Suga, T., Shiio, T., Maeda, Y., and Chihara, G., Antitumor activity of Lentinen in murine syngenic and autochthonous hosts and its suppressive effect on 3-methylcholanthrene-induced carcinogenesis, Cancer Res., 44, 5132-5137,1984. [Pg.621]

Methylcholanthrene-induced (Meth-A) mouse tumor cells grown in an astaxanthin-supplemented medium had reduced cell numbers and lower DNA synthesis rates 1 to 2 days postincubation than control cultures. Similarly, astaxanthin inhibited murine... [Pg.674]


See other pages where Methylcholanthrene-induced is mentioned: [Pg.167]    [Pg.325]    [Pg.336]    [Pg.377]    [Pg.1003]    [Pg.315]    [Pg.509]    [Pg.57]    [Pg.241]    [Pg.270]    [Pg.3]    [Pg.22]    [Pg.123]    [Pg.96]    [Pg.181]    [Pg.622]    [Pg.134]    [Pg.135]    [Pg.172]    [Pg.792]    [Pg.448]    [Pg.207]    [Pg.132]    [Pg.58]    [Pg.120]    [Pg.314]    [Pg.697]    [Pg.706]   


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3-Methylcholanthrene

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