Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.1.17 (ornithine decarboxylase)
 6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure of mouse skin to microwave radiation for 10 sec allows the epidermis to be separated from the dermis by gentle scraping of the skin with a scapel. At the end of the irrradiation period the subcutaneous temperature was 55 degrees C. Histologically, the microwave irradiated skin resembled skin exposed to an established heat separation procedure (i.e., immersion in 55 degrees C water followed by immersion in 0-4 degrees C water). The recoveries of DNA, RNA, and protein on a per area basis were the same for the microwave and conventional heat separation procedures, and the TPA-induced ornithine decarboxylase levels were comparable.
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PMID:Microwave irradiation: a new rapid technique for separating epidermal tissue from mouse skin preserving RNA, DNA, protein and phorbol ester-induced ornithine decarboxylase levels. 33 99

Thyrotropin (TSH) injected intraperitoneally caused a significant rise in the activity of L-ornithine decarboxylase of rat thyroid within 4 hr. TSH-releasing hormone (TRH) also increased the activity of this enzyme in a dose-related manner and of putrescine-activated S-adenosyl-L-methionine decarboxylase, probably through the increased secretion of TSH from the pituitary. Administration of methylthiouracil (MTU) in the drinking water to rats resulted in an increase of these two enzymes in the thyroid. Maximal activation was observed 4 days after the initiation of MTU treatment for both enzymes. The intracellular level of putrescine and spermidine increased during the rapid phase of thyroid enlargement caused by MTU treatment. The spermine concentration, however, was relatively constant during the treatment. The RNA/DNA ratio followed a pattern very similar to that exhibited by the spermidine/spermine ratio. These results indicate that TSH stimulates the biosynthesis of polyamines by increasing the activity of the decarboxylases in the thyroid. The findings further suggest that polyamines play a role in the regulation of thyroid growth and nucleic acid metabolism.
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PMID:Thyroid function and polyamines. II. Thyrotropin stimulation of polyamine biosynthesis in the rat thyroid. 81 58

To challenge the theory of tissue specificity of tumor promoters, the biochemical and tumor promoting effects of okadaic acid (OA), a potent tumor promoter on mouse skin, were studied in the mucosa of rat glandular stomach. OA strongly inhibited protein phosphatases 1 and 2A, and increased 4-fold the phosphorylation of elongation factor 2 in vitro in the mucosa. Intubation of 10 micrograms (12.4 nmol) OA induced ornithine decarboxylase in the mucosa. Tumor promotion of OA was studied in the glandular stomach initiated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in a two-stage carcinogenesis experiment. OA in drinking water, 10 micrograms (12.4 nmol) per rat per day from weeks 9-55 of the experiment, and 20 micrograms (24.8 nmol) from weeks 56-72, significantly enhanced development of the neoplastic changes in the glandular stomach (P < 0.05). The neoplastic changes included adenomatous hyperplasias and adenocarcinomas, both of which correspond to papillomas and carcinomas in a two-stage mouse skin carcinogenesis experiment. The percentages of neoplastic change-bearing rats of the groups treated with MNNG plus OA, MNNG alone or OA alone were 75.0, 46.4 and 0% respectively. OA enhanced tumorigenesis in the MNNG-initiated glandular stomach of rats through the same mechanisms of action as in mouse skin. The OA pathway mediated through inhibition of protein phosphatases 1 and 2A is applicable to various organs as a general mechanism of tumor promotion.
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PMID:An alternative theory of tissue specificity by tumor promotion of okadaic acid in glandular stomach of SD rats. 133 Mar 44

We have recently demonstrated that polyamines are absolutely required for gastric and duodenal mucosal repair after stress. Polyamines act as substrates for transglutaminase and facilitate protein cross-linking. The current study tests whether transglutaminase and protein cross-linking are involved in the mechanism of mucosal healing. Rats were fasted 22 h, placed in restraint cages, and immersed in water to the xiphoid process for 6 h. Animals were killed immediately or 4, 12, or 24 h after stress. Gastric and duodenal mucosa were examined histologically and grossly, and transglutaminase activity was measured. Transglutaminase activity in gastric and duodenal mucosa was increased significantly from 0 to 8 h, peaking 4 h after the 6-h stress period. By 12 h, enzyme activity in duodenal mucosa had returned to control values while gastric mucosal transglutaminase did not decrease to control values until 24 h. Mucosal recovery from lesions produced by stress was evident 12 h after stress and was almost complete by 24 h. Dansylcadaverine (100 mg/kg, orally), a specific inhibitor of protein cross-linking, not only prevented the increases in transglutaminase but significantly decreased healing in both tissues. Oral administration of the polyamine spermidine (100 mg/kg) immediately after stress totally prevented inhibition of repair caused by blocking ornithine decarboxylase with difluoromethylornithine (DFMO, 500 mg/kg). Administration of dansylcadaverine, together with spermidine, significantly prevented the beneficial effect of spermidine on mucosal healing in the DFMO-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of transglutaminase and protein cross-linking in the repair of mucosal stress erosions. 135 Apr 21

The intestinal absorption of aluminum (Al) appears to be enhanced in the uremic rat. Since atrophic changes of the intestinal mucosa have been observed in uremia the present study investigated whether intestinal atrophy induced by difluoromethylornithine (DFMO), a specific inhibitor of ornithine decarboxylase, could affect the absorption of Al. DFMO supplied with the drinking water (5%) to rats with normal renal function for 9 days resulted in a reduced number of microvilli with definite morphological alterations in small intestinal mucosa. Following an oral load of Al urinary excretion rates and 1-hour postload serum concentrations of Al were increased in DFMO-treated rats as compared to controls suggesting enhanced absorption of Al. Pattern and degree of urinary Al excretion as well as ultrastructural alterations of the intestinal mucosa were similar in DFMO-treated rats and uremic rats. The model of DFMO-induced intestinal alterations suggests that structural lesions of the intestine may be involved in the enhanced absorption of Al in uremia.
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PMID:Induction of intestinal mucosal atrophy by difluoromethylornithine: a nonuremic model of enhanced aluminum absorption. 140 1

Rectal mucosal ornithine decarboxylase activity has been reported to distinguish patients with adenomas from normal controls. In order to further explore this association, we assayed biopsy samples from 119 unselected individuals undergoing routine colonoscopic examinations. The overall mean ODC activity was 127.4 (+/- 93.1 SD) pmol/mg protein/hr. There were no differences by age, sex, or race. Tissue handling and storage influenced ODC activity. Specimens collected and transported on Dry Ice had higher ODC activity than specimens initially frozen in a -20 degrees C freezer. After adjusting for storage and collection method, the activity was similar in subjects with adenomas (126.3 pmol/mg/hr) compared to those without adenomas (128.8 pmol/mg/hr). We conclude that variations in assay technique make comparisons between laboratories difficult. Patients with large-bowel adenomas do not necessarily have higher ODC activity in uninvolved rectal mucosa. Further study of the environmental and genetic factors that influence rectal mucosal proliferation may improve our understanding of carcinogenesis in the large bowel.
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PMID:Rectal mucosal ornithine decarboxylase activity is not a useful marker of risk for colorectal neoplasia. 142 72

Our laboratory has been studying cancer chemopreventive effects of polyphenolic fraction isolated from green tea (GTP). In prior studies we have shown that (a) GTP possesses antigenotoxic effects in various test systems; (b) topical application of GTP protects against UV radiation and chemical carcinogen-induced tumorigenesis in murine skin; and (c) feeding of GTP in drinking water p.o. to mice protects against carcinogen-induced forestomach and lung tumorigenesis. Recently, we showed that in a dose-dependent manner GTP inhibits tumor promoter-caused induction of epidermal ornithine decarboxylase activity in SENCAR mice (R. Agarwal et al., Cancer Res., 52: 3582-3588, 1992). In the present study, we assessed the effect of GTP on TPA-induced skin tumor promotion in 7,12-dimethylbenz(a)anthracene-initiated SENCAR mouse. Topical application of varying doses of GTP (1-24 mg) 30 min prior to that of each TPA application resulted in highly significant protection against skin tumor promotion in a dose-dependent manner. The animals pretreated with GTP showed substantially lower tumor body burden such as decrease in total number of tumors per group, number of tumors per animal, tumor volume per mouse, and average volume per tumor, as compared to the animals that did not receive GTP. Since TPA-induced epidermal cyclooxygenase and lipoxygenase activities and edema and hyperplasia are conventionally used markers of skin tumor promotion, we also assessed the effect of preapplication of GTP on these parameters. As quantitated by the formation of prostaglandin and hydroxy-eicosatetraenoic acid metabolites from, respectively, cyclooxygenase- and lipoxygenase-catalyzed metabolism of arachidonic acid, skin application of GTP to SENCAR mice resulted in significant inhibition of TPA-caused effects on these 2 enzymes. Prior application of GTP to mouse skin also resulted in 30-46% inhibition of TPA-induced epidermal edema and hyperplasia. The results of the present study suggest that GTP possesses anti-skin tumor-promoting effects, and that the mechanism of such effects may involve inhibition of tumor promoter-induced epidermal ornithine decarboxylase, cyclooxygenase and lipoxygenase activities, edema, and hyperplasia. Further studies are in progress to define which component present in GTP is responsible for its anti-skin tumor-promoting effects.
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PMID:Inhibition of 12-O-tetradecanoylphorbol-13-acetate-caused tumor promotion in 7,12-dimethylbenz[a]anthracene-initiated SENCAR mouse skin by a polyphenolic fraction isolated from green tea. 145 78

The effects of palm carotene on chemical carcinogenesis was studied. Palm carotene suppressed mouse epidermal ornithine decarboxylase activity induced by glycocholic acid. In a two-stage mouse epidermal carcinogenesis experiment using 7,12-dimethylbenz(a)anthracene as the initiator, glycocholic acid as the 1st stage promoter, and mezerein as the 2nd stage promoter, palm carotene inhibited the promoting activity of glycocholic acid. Furthermore, in N-ethyl-N'-nitro-N-nitrosoguanidine-induced mouse duodenal carcinogenesis, 0.05% of palm carotene given in drinking water decreased the percentage of tumor-bearing mice significantly.
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PMID:Palm carotene inhibits tumor-promoting activity of bile acids and intestinal carcinogenesis. 146 91

The compound 5'-([(Z)-4-amino-2-butenyl]methylamino)-5'-deoxyadenosine (MDL73811), a potent inhibitor of S-adenosylmethionine decarboxylase, was effective in mice against six of eight clinical isolates of Trypanosoma brucei rhodesiense, the causative agent of East African sleeping sickness. In combination with the ornithine decarboxylase inhibitor DL-alpha-difluoromethylornithine (DFMO; Ornidyl), MDL73811 acted synergistically to cure seven of eight infections. MDL73811 was effective when given singly at 50 to 100 mg/kg of body weight per day for 7 days (osmotic pumps). In combination with subcurative DFMO levels (0.25 to 1.0% in drinking water for 7 days), the curative MDL73811 dose could be lowered to 25 or 50 mg/kg, depending on the isolate. Oral administration of the MDL73811-DFMO combination was also effective in an acute infection and in a long-term central nervous system model of Trypansoma brucei brucei infection. These data indicate that MDL73811 may be effective therapeutically in drug-refractory and late-stage East African trypanosomiasis.
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PMID:Cure of murine Trypanosoma brucei rhodesiense infections with an S-adenosylmethionine decarboxylase inhibitor. 148 41

The aim of the present study was to evaluate in vivo the role of polyamines in the secretion of atrial natriuretic peptide (ANP). alpha-Difluoromethylornithine (DFMO) which inhibits ornithine decarboxylase activity and polyamine synthesis was given in drinking water and through intraperitoneal administration to Sprague-Dawley rats. Carotid artery was cannulated for collection of blood samples and measurement of blood pressure following the administration of arginine-vasopressin (AVP). Analysis of polyamines in cardiac tissue indicated that DFMO treatment decreased contents of putrescine and spermidine in cardiac tissue by 80% and 48%, respectively. Quantitation of ANP in plasma by radioimmunoassay indicated that both basal and stimulated levels of ANP in DFMO-treated animals were 21.5% and 50% of those in control rats. The administration of putrescine restored the levels of basal and AVP-stimulated levels of ANP in plasma which confirmed that DFMO effect on ANP secretion occurred specifically through the polyamine pathway.
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PMID:Inhibition of polyamine synthesis impairs the secretion of atrial natriuretic peptide. 153 63


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