Ornithine decarboxylase induction

Caldwell, K. A., Grosjean, O. K., Henika, P. R., Friedman, M. (1991). Hepatic ornithine decarboxylase induction by potato glycoalkaloids in rats. Food Chem. Toxicol, 29, 531-535. 

Fischer, S.M., Baldwin, J.K., Jasheway, R.W., Patrick, K.E., and Cameron, G.S., Phorbol ester induction of 8-hpoxygenase in inbred SENCAR (SSIN) but not C57BL/6J mice correlated with hyperplasia, edema, and oxidant generation by not ornithine decarboxylase induction. Cancer Res., 48, 658, 1988. 

O-tetradecanoyl-phorbol-l 3-acetate-caused epidermal ornithine decarboxylase induction and tumor promotion in relation to lipoxygenase inhibition by these compounds, Gann, 75,214-222, 1984. 

Monks, T.J., S.E. Walker, L.M. Flynn, C.J. Conti, and J. DiGiovanni. 1990. Epidermal ornithine decarboxylase induction and mouse skin tumor promotion by quinones. Carcinogenesis 11(10) 1795-1801. 

H2O2 plays a major role in asbestos-stimulated ornithine decarboxylase induction. 

Okai, Y, Higashi-Okai, K., Yano, Y, Otani, S., 1996. Suppressive effects of chlorophyllin on mutagen-induced umu C gene expression in Salmonella typhimurium (TA 1535/pSK 1002) and tumor promoter-dependent ornithine decarboxylase induction in BALB/c 3T3 fibroblast cells. Mutation Research/Genetic Toxicology 370 (1), 11-17. 

MAJUMDAR A p (1990) Role of tyrosine kinases in gastrin induction of ornithine decarboxylase in colonic mucosa. Am J Physiol. 259 (4 Ptl) G626-G630. 

Guyton, K. Dolan, P. M. Kensler, T. W. Quinone methide mediates in vitro induction of ornithine decarboxylase by the tumor promoter butylated hydroxytoluene hydroperoxide. Carcinogenesis 1994, 15, 817-821. 

Administration of single oral doses of 90 or 120 mg/kg mirex by gavage to female Sprague-Dawley rats resulted in induction of hepatic ornithine decarboxylase activity there was, however, no evidence of significant damage to deoxyribonucleic acid (DNA) as measured by alkaline elution (Mitra et al. 1990). 

In animal studies, mirex (a nonmutagenic hepatocarcinogen) promoted mouse skin squamous carcinomas and papillomas after initiation with 7,12-dimethyl-benz[a]anthracene (DMBA) for 1 week. Mirex, also, potentiated the promotional potency of the phorbol ester tumor promoter, 12-0 -tetradecanoylphorbol-13-acetate (TPA). There was a 90% incidence (activation) of the c-Ha-ras tumor gene in these co-promoted tumors. When both mirex and TPA gave a similar tumor yield, only the TPA response was associated with biochemical markers of enhanced cell proliferation, induction of epidermal ornithine decarboxylase activity and increased DNA synthesis, and hyperplasia. Thus, there is evidence for a dual effect of mirex during co-promotion first, as an independent tumor promoter with a mechanism different than that of phorbol esters and second, as a compound that also potentiates skin tumor promotion by TPA (Meyer et al. 1993, 1994 Moser et al. 1992, 1993). 

Endo Y Simultaneous induction of histidine and ornithine decarboxylases and changes in their product amines following the injection of Escherichia coli lipopolysaccharide into mice. Biochem Pharmacol 1982 31 1643-1647. 

Savage RE Jr., Pereira MA, DeAngelo AB. 1988. Chloroform induction of ornithine decarboxylase antizyme (ODC-AZ) in male rat liver. J Toxicol Environ Health 1 97-101. 

Savage RE Jr., Westrich C, Guion C, et al. 1982. Chloroform induction of ornithine decarboxylase activity in rats. Environ Health Perspect 46 157-162. 

Epstein-Barr virus early antigen induction. Methanol extract of the dried leaf, in cell culture at a concentration of 1 pg/mL, was inactive. The assay was designed for tumor-promoting activity . Two diastere-oisomers of 2,7,1 l-cembratriene-4,6-diol (a- and 3-CBT) from the neutral fractions of cigarette smoke condensate, in Raji cells, produced potent inhibitory effects on the induction of Epstein-Barr virus (EBV)-EA by 12-0-tetradecanoylphorbol-13-acetate (TPA). The doses of a- and P-CBT required for 50% inhibition of EBV-EA induction by TPA were 7.7 and 6.7 mg/mL, respectively. Application of a- and P-CBT to mouse skin before treatment with TPA, inhibited TPA-induced ornithine decarboxylase activity in a dose-dependent manner. Application of 16.5 pM/mouse of a- and p-CBT resulted... 

Furihata, C., Hatta, A. Matsushima, T. (1989) Inductions of ornithine decarboxylase and replicative DNA synthesis but not DNA single strand scission or unscheduled DNA synthesis in the pyloric mucosa of rat stomach by catechol. Jpn. J. Cancer Res., 80. 1052-1057... 

The mechanisms by which antitumor-promoters suppress the tumor promotion are not known, but may be due to the following effects (i) inhibition of polyamine metabolism (ii) inhibition of arachidonic acid metabolism (iii) protease inhibition (iv) induction of differentiation (v) inhibition of oncogene expression (vi) inhibition of PKC and (vii) inhibition of oxidative DNA damage [3,6,91]. The polyamine content of cells is correlated to their proliferative, and often, their neoplastic capabilities. A key enzyme in the polyamine biosynthetic pathway, ornithine decarboxylase (ODC), catalyzes the convertion of ornithine to putrescine. Phorbol ester promoters such as TPA cause increased ODC activity and accumulation of polyamines in affected tissues. Diacylglycerol activated PKC, and the potent tumor promoter, TPA, binds to, and activates PKC, in competition with diacylglycerol. PKC stimulation results in phosphorylation of regulatory proteins that affect cell proliferation. Some chemopreventive agents have inhibitory activity towards PKC. Refer to recent review articles for further discussion [3,6,91]. 

Huang et al. [70] have evaluated the effects of chlorogenic acids on tumor promotion in an animal study using CD-I mice. Chlorogenic, caffeic and ferulic acids inhibit the induction of ornithine decarboxylase by 12-O-tetradecanoylphorbol-13-acetate (TPA). TPA-mediated DNA synthesis has been weakly inhibited, but TPA-induced skin tumor promotion has been markedly inhibited by these compounds. 

White EL, Ross LJ, Schmid SM, Kelloff GJ, Steele VE, Hill DL. 1998a. Screening of potential cancer-preventing chemicals for inhibition of induction of ornithine decarboxylase in epithelial cells from rat trachea. Oncol Rep 5 717-722. 

Lombardi G., Szekely A. M., Bristol L. A., Guidotti A., and Manev H. (1993). Induction of ornithine decarboxylase by N-methyl-D-aspartate receptor activation is unrelated to potentiation of glutamate excitotoxicity by polyamines in cerebellar granule neurons. J. Neurochem. 60 1317-1324. 

Reed L. J. and De Belleroche J. (1990). Induction of ornithine decarboxylase in cerebral cortex by excitotoxin lesion of nucleus basalis association with postsynaptic responsiveness and N-methyl-D-aspartate receptor activation. J. Neurochem. 55 780-787. 

Ornithine decarboxylase (ODC) is the first enzyme in the polyamine biosynthesis pathway. Polyamines play essential roles in cell proliferation and differentiation and participate in macromolecular synthesis. Inhibitors of ODC block aspects of tumor promotion and induce cellular differentiation in several animal carcinogenesis models. Thus induction of ODC has been implicated as being important to carcinogenesis, and ODC activity is an intermediate biomarker of cell proliferation in studies... 

GH has been shown to induce a number of enzymes concerned with amino acid metabolism in the liver of the hypophysectomized rat (in vivo or in perfused liver [78]). Induced enzymes include tyrosine aminotransferase, tryptophan oxygenase and ornithine decarboxylase. The effects are complex, particularly in relation to interaction with glucocorticoids, and in some experiments GH lowered enzyme levels induced by glucocorticoids, although given alone it led to induction of these enzymes. 

IMANISHI, S., HASHIZUME, K., NAKAKITA, M., KOJIMA, H MATSUBAYASHI, Y., HASHIMOTO, T., SAKAGAMI, Y., YAMADA, Y NAKAMURA, K., Differential induction by methyl jasmonate of genes encoding ornithine decarboxylase and other enzymes involved in nicotine biosynthesis in tobacco cell cultures. Plant Mol. Biol., 1998,38,1101-1111. 

Recent developments in cellular biology have demonstrated the important role of mitogenic signal transduction in controlling the tumor proliferation. The induction of ornithine decarboxylase (ODC), PKC, protein kinase activities, and oxidative stress by the phorbol ester, TPA, is believed to be closely related to the tumor promotion activity of this compound. Topical application of green tea polyphenols to mouse skin was found to inhibit TPA-caused induction of ODC activity in a dose-dependent manner. Our studies demonstrated that EGCG and TF-3 inhibited TPA-induced transformation, PKC activation, and AP-1 binding activities in mouse fibroblast cells. ... 

Argarwal, R., Katiyar, S.K., Zaidi, SLA, and Mukhtar, H., Inhibition of tumor promoter-caused induction of ornithine decarboxylase activity in Senear mice by phenolic fraction isolated from green tea and its individual epicatechin derivatives, Cancer Res., 52, 3582-3588, 1992. 

Bonchev, D., Seitz, W.A., Mountain, CF. and Balaban, A.T. (1994b). Modeling the Anticarcino-genic Action of Retinoids by Making Use of the OASIS Method. 3. Inhibition of the Induction of Ornithine Decarboxylase by Arotinoids. J.Med.Chem.,37,2300-2307. [R]... 

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