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TPA induced ornithine decarboxylase

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... [Pg.308]

Effects of Retinoids on TPA-induced Ornithine Decarboxylase and Transglutaminase Activity... [Pg.242]

LaHann concluded that capsaicin appeared to facilitate the onset of TPA-induced tumorigenesis and that capsaicin might increase the risk of skin cancer. In the studies of Sasajima et al., capsaicin induced ornithine decarboxylase (ODC) activity, an enzyme used as an index of tumor promoting capability. There appears to be sufficient evidence that capsaicin may pose a tumorigenic threat. [Pg.365]

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]

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. [Pg.937]

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]

Agarwal, R. et al.. Inhibitory effect of silymarin an antihepatotoxic flavonoids on TPA-induced epidermal ornithine decarboxylase activity and mRNA in SENCAR mice. Carcinogenesis, 15, 1099, 1994. [Pg.105]

Studies of the methanolic extract of Alpinia oxyphylla have shown that this extract suppresses the promotion of skin tumors in mice and that it induces apoptosis in cultured human promyelocytic leukemia cells. In addition, two phenolic diarylheptano ids isolated from the active extract, yakuchinone A and yakuchinone B, were found to ameliorate tumor promotion as well as inhibit both TPA-induced epidermal ornithine decarboxylase (ODC) activity and ODC RNA expression. Moreover, yakuchinones A and B reduced production of the TNF-a in the TPA-stimulated skin of mice. Furthermore, both compounds inhibited the TPA-induced expression of COX-2 at both transcriptional and... [Pg.169]

The MeOH extract of Rosmarinus officinalis (Lamiaceae) contains 16-20% of ursolic acid. Both the extract and the pure triterpene isolated from it were strong inhibitors of TPA-induced inflammation, ornithine decarboxylase (ODC) activity and tumour promotion in mouse skin. Some authors have suggested that the effects could be related to those of... [Pg.124]

Caffeic Acid Phenethyl Ester (CAPE). CAPE, a phenolic compound with antioxidant properties, is an active ingredient derived from honeybee propolis (52). CAPE has antiviral, anti-inflammatory and antiproliferative properties. The compound differentially suppresses the growth of numerous human cancer cells and also inhibits tumor promoter-mediated processes in transformed cells (53,54). In transformed cells, CAPE induces apoptosis and inhibits the expression of the malignant phenotype (55,56). In addition, CAPE treatment attenuates the formation of azoxymethane-induced aberrant crypts and the activities of ornithine decarboxylase (ODC), tyrosin protein kinase, and lipoxygenase activity (57). Although the molecular basis for these multiple chemopreventive effects of CAPE is not clear, recent studies have demonstrated that CAPE is a potent and specific inhibitor of the transcription factor NF-kB (58). CAPE inhibited the activity and expression of COX-2 in the carrageenan air pouch model of inflammation as well as in TPA-treated human oral epithelial cells (59). CAPE was able to reduce neointimal formation by inhibiting NF-kB activation in a model of endothelial injury of rat carotid artery (60). [Pg.158]

Inhibition of TPA-Induced tumor promotion and ornithine decarboxylase activity Quercetin 10-30 lunole/mouse applied to skin 39... [Pg.515]

Like many other antioxidants, rosemary and its polyphenols possess not only antioxidative activities, but also antitumorigenic activities. Huang et al. (5) investigated the inhibitory effects of rosemary extract, carnosol and ursolic acid on tumor formation in mouse skin. They found that topical application of rosemary inhibits B(a)P- and DMBA-induced initiation of tumor and TPA-induced tumor promotion in DMBA-initiated mice. Carnosol and ursolic acid were found to be strong inhibitors of TPA-induced inflammation, ornithine decarboxylase activity and tumor promotion in mouse skin (5). It was suggested that carnosol acted like other nonsteroidal phenolic anti-inflammatory agents, such as curcumin, which inhibited the metabolism of arachidonic acid. [Pg.82]


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