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Ornithine decarboxylase ODC

Biosynthesis of polyamines is essential for growth and multiplication of T. brucei, hence discovery of drug candidates that inhibit enzymes in the polyamine biosynthesis pathway represent an attractive approach to development of trypanocides. The consequences of gene knockout of ornithine decarboxylase (ODC), the target of eflornithine (3), have been further characterized and suggest that new inhibitors of this enzyme may be particularly effective [18]. [Pg.280]

The 26S proteasome also degrades non-ubiquitylated proteins [71]. The short-lived enzyme ornithine decarboxylase (ODC) and the cell-cycle regulator p21Cip provide well documented examples of ubiquitin-independent proteolysis by the 26S en-... [Pg.230]

Savage RE Jr., DeAngelo AB, Guion C, et al. 1987. Studies on the mechanism of action of chloroform stimulation of rat hepatic ornithine decarboxylase (ODC). Res Commun Chem Pathol Pharmacol 58 97-113. [Pg.284]

Aminooxy compounds can be viewed as O-ethers of HA and are discussed here in terms of their potential anticancer activity. Thus, l-aminooxy-3-aminopropane (APA) is a potent reversible inhibitor of mammalian ornithine decarboxylase (ODC) and of S-adenosylmethionine decarboxylase (SAMDC) , and 6 -(5 -deoxy-5 -adenosyl)methylsul-fonium 0-ethylhydroxylamine (AMA) was reported to be an efficient reversible inhibitor of the latter enzyme . [Pg.628]

It was documented in several studies that high doses of p-carotene lead to a downregulation of ornithine-decarboxylase (ODC) in patients... [Pg.201]

Metabolism of polyamines has a direct action on cell proliferation. Thus, it is a therapeutic target for the design of antitumor agents. However, inhibition of ornithine decarboxylase (ODC) by specific inhibitors does not completely cancel the activity. This is due to the existence of other biosynthetic pathways (i.e., SAM-DC). These pathways are themselves regulated by polyamines. [Pg.270]

Effect of CLA on Protein Kinase C (PKC) Activity. 12-0-tetradecanoylphorbol-13-acetate (TPA) administered by gavage induced the activity of ornithine decarboxylase (ODC) in a similar manner to that observed in mouse skin (28). The peak activity was about 5-times control and occurred 6 hrs after TPA intubation. Treating mice with CLA (100 mg p. o., twice per week) for 1, 2 or 4 weeks progressively reduced the TPA... [Pg.269]

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]. [Pg.66]

Resveratrol exerts antitumor effects partly by arresting the growth of various cancer cells in culture [Kundu and Surh, 2004]. The inhibition of ornithine decarboxylase (ODC), a biochemical hallmark of tumor promotion, has been shown to account for the antiproliferative and antitumor effects of resveratrol [Schneider et al., 2000 Ulrich et al., 2007]. Aberrant changes in cell-cycle machinery are considered as the biochemical basis of abnormal proliferation of transformed cells. Major cell-cycle regulatory proteins include various cyclins, cyclin-dependent kinases (Cdk), Cdk inhibitors, and check point kinases (Chkl... [Pg.341]

Ornithine decarboxylase catalyzes the transformation of ornithine to the polycationic bases, putresine, spermine, and spermidine. These compounds exert regulatory effects on cell growth. It has been shown that quercetin (10 to 30 pmol/mouse) markedly suppressed the stimulatory effect of the transporters associated with antigen processing (TPA) on ornithine decarboxylase (ODC) activity and on skin tumor formation in mice initiated with dimethylbenzanthracene. Such inhibition may be related to the activation of the catalytic site, which is under nonconventional regulation by small molecules. Also, the synthetic flavonoid flavone acetic acid was shown to inhibit the activity of ODC in stimulated human peripheral blood lymphocytes and human colonic lamina propria lymphocytes. [Pg.334]

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... [Pg.79]

The V-methyl -A1 -pyrrol ini um cation is the last common intermediate in both TA and nicotine biosynthesis (Fig.7.4). V-Methy 1-A1 -pyrrolinium cation formation begins with the decarboxylation of ornithine and arginine by ornithine decarboxylase (ODC) and arginine decarboxylase (ADC), respectively. Putrescine is formed... [Pg.151]

The concept of inhibition via p elimination of fluoride ion has now been extended to the irreversible inhibition of a-amino acid decarboxylases. Ornithine decarboxylase (ODC), which catalyzes the decarboxylation of ornithine to putrescine is irreversibly inhibited by a-difluoromethylornithine (IX Fig. 9) (28). In this case, the carbanion formation which precedes P elimination is generated by loss of CO2, and not by proton abstraction (Fig. 9). Similarly, aromatic amino acid decarboxylase is irreversibly inhibited by C-difluoromethyl-3,4-dihydroxyphenylalanine (29) while histidine decarboxylase, ornithine decarboxylase and aromatic amino acid decarboxylase have been inhibited by the corresponding <=d-monof luoromethylanri.no acids, respectively (29). [Pg.248]

Figure 7.16 Phylogenetic relationships in key enzymes of pathways leading to SM, based on amino acid sequences, (a) Ornithine decarboxylase (ODC). (b) Tyrosine decarboxylase (TyrDC). (c) Tryptophan decarboxylase (TDC). (d) Phenylalanine ammonia-lyase (PAL). Numbers at nodes are bootstrap values. Figure 7.16 Phylogenetic relationships in key enzymes of pathways leading to SM, based on amino acid sequences, (a) Ornithine decarboxylase (ODC). (b) Tyrosine decarboxylase (TyrDC). (c) Tryptophan decarboxylase (TDC). (d) Phenylalanine ammonia-lyase (PAL). Numbers at nodes are bootstrap values.
Table 7.2 Sequence alignment (amino acids) of ornithine decarboxylase (ODC) of selected taxa from plants, animals, fungi and bacteria. Conserved sites are marked by x ... Table 7.2 Sequence alignment (amino acids) of ornithine decarboxylase (ODC) of selected taxa from plants, animals, fungi and bacteria. Conserved sites are marked by x ...
We first assessed the effects of apigenin on ornithine decarboxylase (ODC) activity, a marker of cell proliferation, in cultured human colon cancer cells (Caco-2). ODC activity was measured by assessing the release of CO2 from 1-C -ornithine. Apigenin treatment for 15 to 39 h at 10 or 30 pM inhibited the ODC in the cultured colonic Caco-2 cells by 26 5 and 57 12%, respectively, when compared with the vehicle (p < 0.01). Studies in CF-1 mice determined dietary apigenin effects on ODC and ACF, precursors of colon cancer. These studies in mice demonstrated that dietary apigenin fed at 0.1 % for 1 week reduced the colonic basal ODC activity by 42 23% in comparison with control diet (p < 0.01). Because ODC was inhibited by only 1 week of dietary apigenin at... [Pg.67]

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. ... [Pg.87]

The first key step in the biosynthesis of tropane alkaloids is the formation of the intermediate putrescine. Polyamines and, therefore putrescine, are found in plant cells and are implicated in growth, root, fruit and flower development, and in different stress phenomena. It is well known that plants synthesize polyamines from ornithine and arginine, unlike other eukaryotes like mammals, which only synthesize polyamines from ornithine. In plants putrescine is synthesized directly from ornithine, a reaction catalysed by ornithine decarboxylase (ODC, EC 4.1.1.17) and indirectly from arginine via agmatine catalysed by arginine decarboxylase (ADC, EC 4.1.1.19), Fig. (1). In Arabidopsis, it is known that the adc gene is required for the production of polyamines that are essential for normal seed development [103]. [Pg.329]


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See also in sourсe #XX -- [ Pg.25 , Pg.45 , Pg.66 ]




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