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

We report induction of renal growth and injury in the intact rat kidney using a diet deficient in vitamin E and selenium. This diet was imposed in 3-wk-old male weanling rats, and after 9 wk, enhancement of growth, characterized by increased wet weight, dry weight, protein content, and DNA content appeared. Morphometric analyses revealed increased kidney volume, tubular epithelial volume, and mean glomerular volume. There were no differences in nephron number. The animals on the deficient diet displayed increased urinary protein excretion at 9 wk. Renal injury was also characterized by an interstitial cellular infiltrate and diminutions in glomerular filtration rate. Enhanced growth and injury were antedated by increased renal ammoniagenesis. The deficient diet did not induce metabolic acidosis, potassium depletion, glucose intolerance, or elevated plasma amino acid concentration. Enhancement of renal growth and ammoniagenesis by the deficient diet was not suppressible by chronic alkali therapy. Stimulation of renal growth could not be ascribed to increased intrarenal iron, induction of ornithine decarboxylase, or alterations in glomerular hemodynamics. Stimulation of renal ammoniagenesis by dietary deficiency of antioxidants is a novel finding, as is induction of growth and injury. We suggest that increased renal ammoniagenesis contributes to induction of renal growth and injury.
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PMID:Induction of renal growth and injury in the intact rat kidney by dietary deficiency of antioxidants. 221 7

A progressive increase in intestinal 59Fe3+ absorption was observed on oral feeding of mice with physiological doses of EGF/UGO. Maximal changes were apparent after 3d and appeared to be dose-dependent. In addition to a small increase in intestinal cell proliferation, as reflected by increased ornithine decarboxylase activity, EGF/UGO-feeding increased mucosal permeability (evaluated with [51Cr]-EDTA): the latter could account for the increase in iron absorption. Sialoadenectomy, to remove the major source of endogenous EGF/UGO, had no appreciable effect on the intestinal absorption of iron.
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PMID:Effect of orally-administered epidermal growth factor on intestinal iron absorption and mucosal permeability. 267 28

Escherichia fergusonii (formerly known as Enteric Group 10) and Enterobacter taylorae (formerly known as Enteric Group 19) are proposed as new species in the family Enterobacteriaceae. By DNA hybridization (32P, 60 degrees C, hydroxyapatite), strains of E. fergusonii were 90 to 97% related to the type strain (holotype) ATCC 35469. They were most closely related to Escherichia coli and more distantly related to species in other genera. E. fergusonii strains are positive for indole production, methyl red, lysine decarboxylase, ornithine decarboxylase, and motility. They ferment D-glucose with gas production and also ferment adonitol, L-arabinose, L-rhamnose, maltose, D-xylose, trehalose, cellobiose, and D-arabitol. They are negative for Voges-Proskauer, citrate utilization (17% positive), urea hydrolysis, phenylalanine deamination, arginine dihydrolase, growth in KCN, and fermentation of lactose, sucrose, myo-inositol, D-sorbitol, raffinose, and alpha-methyl-D-glucoside. By DNA hybridization (32P, 60 degrees C, hydroxyapatite), strains of E. taylorae were 84 to 95% related to the type strain (holotype) ATCC 35317. Their nearest relative was E. cloacae, to which they were 61% related. Other named species were more distantly related. Strains of E. taylorae are positive for Voges-Proskauer, citrate utilization, arginine dihydrolase, ornithine decarboxylase, motility, growth in KCN medium, and malonate utilization. They ferment D-glucose with gas production and also ferment D-mannitol, L-arabinose, L-rhamnose, maltose, D-xylose, trehalose, and cellobiose. They are negative for indole production, methyl red, H2S production on triple sugar-iron agar, urea hydrolysis, phenylalanine deamination, lysine decarboxylase, gelatin hydrolysis, and fermentation of adonitol, i-inositol, D-sorbitol, and raffinose. Both new species occur in human clinical specimens. Two strains of E. fergusonii were isolated from blood. Five stains of E. taylorae were isolated from blood, and one was from spinal fluid. These blood and spinal fluid isolates suggest possible clinical significance, but this point requires further study.
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PMID:Escherichia fergusonii and Enterobacter taylorae, two new species of Enterobacteriaceae isolated from clinical specimens. 396 4

When rat liver homogenate or its postmitochondrial supernatant was incubated with L-cysteine, but not D-cysteine, ornithine decarboxylase (ODC) lost more than half of its catalytic activity within 30 min and, at a slower rate, its immunoreactivity. The inactivation correlated with production of H2S during the incubation. These changes did not occur in liver homogenates from vitamin B6-deficient rats. A heat-stable inactivating factor was found in both dialysed cytosol and washed microsomes obtained from the postmitochondrial supernatant incubated with cysteine. The microsomal inactivating factor was solubilized into Tris/HCl buffer, pH 7.4, containing dithiothreitol. Its absorption spectrum in the visible region resembled that of Fe2+ X dithiothreitol in Tris/HCl buffer. On the other hand FeSO4 inactivated partially purified ODC in a similar manner to the present inactivating factor. During the incubation of postmitochondrial supernatant with cysteine, there was a marked increase in the contents of Fe2+ loosely bound to cytosolic and microsomal macromolecules. Furthermore, the content of such reactive iron in the inactivating factor preparations was enough to account for their inactivating activity. These data suggested that H2S produced from cysteine by some vitamin B6-dependent enzyme(s) converted cytosolic and microsomal iron into a reactive loosely bound form that inactivated ODC.
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PMID:Cysteine-dependent inactivation of hepatic ornithine decarboxylase. 669 45

Kluyvera is proposed as a new genus for the group of organisms formerly known as Enteric Group 8 (synonym = API group 1). Strains of Kluyvera share the properties of most members of the family Enterobacteriaceae: they are gram-negative rods, motile with peritrichous flagella, catalase positive, and oxidase negative; they grow on MacConkey agar, ferment D-glucose with the production of acid and gas, and are susceptible to many antibiotics. Strains are usually indole positive, methyl red positive, Voges-Proskauer negative, citrate positive, H2S (triple sugar iron) negative, urea negative, phenylalanine deaminase negative, lysine decarboxylase positive, arginine dihydrolase negative, and ornithine decarboxylase positive. Kluyvera strains ferment many of the sugars and polyhydroxyl alcohols used in identification. By deoxyribonucleic acid-deoxyribonucleic acid hybridization, strains of Kluyvera were divided into three groups. Kluyvera ascorbata is proposed as the type species for the genus. Most strains of K. ascorbata have been isolated from clinical specimens. K. cryocrescens is proposed as the second species. It was occasionally isolated from clinical specimens, but it was isolated more commonly from the environment. Kluyvera species group 3 was heterogeneous, but was distinct from the two named species by deoxyribonucleic acid hybridization. This group was rare, so no species name will be proposed at this time. K. ascorbata can be differentiated from K. cryocrescens by its positive ascorbate test, inability to grow at 5 degrees C in a refrigerator, and smaller zones of inhibition around carbenicillin and cephalothin disks. The test normally used for identification does not clearly differentiate these two species. Kluyvera species are probably infrequent opportunistic pathogens. The most common source is sputum, where they are probably not clinically significant. Five strains have been from blood cultures. More information is needed about the incidence and clinical significance of the genus Kluyvera.
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PMID:Kluyvera, a new (redefined) genus in the family Enterobacteriaceae: identification of Kluyvera ascorbata sp. nov. and Kluyvera cryocrescens sp. nov. in clinical specimens. 724 Apr 3

An abbreviated procedure for the biochemical identification of Yersinia enterocolitica isolated from food enrichments on CIN (cefsulodin-irgasan-novobiocin) agar was investigated. A total of 170 colonies resembling Y. enterocolitica in colonial morphology and appearance on CIN agar were selected for identification using API strips. Ninety-three of these isolates were examined with the PathoTec ornithine decarboxylase, Voges-Proskauer, and urease test strips. The PathoTec urease strip alone was adequate for identification of all isolates of Y. enterocolitica. Christensen's urea agar was applied to the remaining 77 isolates and found less specific in the 1 isolate of Enterobacter agglomerans was urease positive along with 10 isolates of Y. enterocolitica. CIN agar is a highly specific medium for isolation of Y. enterocolitica, requiring only Kligler iron agar and urea slants for confirmation of presumptive colonies.
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PMID:An abbreviated scheme for identification of Yersinia enterocolitica isolated from food enrichments on CIN (cefsulodin-irgasan-novobiocin) agar. 730 81

This study was undertaken to estimate if dietary iron could stimulate factors which promote spontaneous lung tumorigenesis in A/J mice, by measuring biochemical parameters of oxidative stress on pulmonary nuclei, ornithine decarboxylase (ODC) and spermidine/spermine N1-acetyltransferase (SAT) activities as markers of tumor promotion. Feeding excessive iron (500%) to A/J mice for 28 weeks significantly elevated pulmonary DNA single strand break (DNA-SSB) as well as nuclear thiobarbituric acid reactive substances (TBARS) in connection with the increase of nuclear nonheme iron level. In contrast, nuclear alpha-tocopherol levels in the iron-loaded group significantly decreased as compared to that in the control group. Pulmonary ODC and SAT activities showed increasing tendency on feeding excess iron for 28 weeks. These results suggest that dietary iron stimulates spontaneous lung tumor promotion in A/J mice, partly due to the enhancement of oxidative damage to the pulmonary nuclei.
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PMID:Stimulating effect of excess iron feeding on spontaneous lung tumor promotion in mice. 759 32

m-Chloroperoxybenzoic acid (CPBA) was tested for its ability to induce the ornithine decarboxylase (ODC) marker of skin tumor promotion. In contrast to benzoyl peroxide, dicumyl peroxide, and 2-butanol peroxide, 5 mg of CPBA applied twice at a 72-h interval induce ODC activity at least as much as 3 micrograms of 12-O-tetradecanoylphorbol-13-acetate (TPA). ODC induction peaks 36 h after a single CPBA treatment but is maximal 5 h after two applications of CPBA at a 48-h interval. The ODC-inducing activity of CPBA is dose dependent and sustained after chronic treatment. In contrast to TPA, two CPBA treatments at 12-24 h intervals produce no refractory state against ODC induction. The mechanism of ODC induction by CPBA is iron dependent. Various hydrolyzable tannins, condensed tannins (CTs) and their monomeric units remarkably inhibit the ODC response to multiple CPBA treatments. At 12 mg, gallic acid, Aleppo gall tannic acid (TA), catechin, and loblolly pine bark CT inhibit the most CPBA-induced ODC activity. Aleppo gall TA is even effective when applied several hours before CPBA. The tumor-promoting activity of CPBA and its inhibition by plant tannins remain to be evaluated.
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PMID:Ability of m-chloroperoxybenzoic acid to induce the ornithine decarboxylase marker of skin tumor promotion and inhibition of this response by gallotannins, oligomeric proanthocyanidins, and their monomeric units in mouse epidermis in vivo. 765 98

Asbestos fibers are potent elaborators of active oxygen species whether by reactions involving iron on the surface of the fiber, or by attempted phagocytosis of fibers by cell types resident in the lung. The link between production of active oxygen species and the pathogenesis of asbestos-mediated disease has been highlighted by studies outlined here exploring the use of antioxidant scavengers which inhibit the cytotoxic effects of asbestos both in vitro and in vivo. The use of antioxidant enzymes ameliorates the induction of certain genes necessary for cell proliferation, such as ornithine decarboxylase, implicating oxidants as causative factors in some abnormal cell replicative events. Based on these observations, antioxidant enzymes likely represent an important lung defense mechanism in response to oxidative stress. In addition, their gene expression in lung or in cells from bronchoalveolar lavage might be a valuable biomarker of chronic inflammation and pulmonary disease after inhalation of oxidants.
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PMID:Oxygen radicals and asbestos-mediated disease. 770 83

Metabolism of the skin tumor promoter butylated hydroxy-toluene hydroperoxide (2,6-di-tert-butyl-4-hydroperoxyl-4-methyl-2,5-cyclohexadienone; BHTOOH) to reactive intermediates is required for tumor promotion by this compound. In particular, an electrophilic quinone methide is known to mediate both in vivo tumor promotion as well as in vitro cytotoxicity by BHTOOH. In the present study, the role of this reactive intermediate in the induction of ornithine decarboxylase (ODC), a gene strongly associated with tumor promotion, was investigated in cultured keratinocytes. BHTOOH stimulates a time-dependent increase in ODC enzyme activity, paralleled by ODC mRNA induction, suggesting transcriptional regulation of ODC by BHTOOH. Depletion of intracellular glutathione caused a 5-fold potentiation of keratinocyte sensitivity to BHTOOH. Concordantly, ODC induction by BHTOOH could be completely inhibited by soluble thiol compounds. These results suggest that ODC induction is mediated by a thiol-reactive metabolite of BHTOOH. The iron-specific chelator desferal blocked ODC induction by BHTOOH, indicating that formation of this intermediate is iron-dependent. Substitution of the 4-methyl group of BHTOOH with alkyl groups of incrementally larger size is known to reduce accordingly quinone methide production; comparative study of these BHTOOH analogs demonstrated a corresponding loss of potency for ODC induction, indicating that BHT-quinone methide mediates the in vitro induction of ODC by BHTOOH. Finally, kinase inhibitor studies suggested a role for protein kinase C in the induction of ODC by BHTOOH. Taken together, these results provide insight into the cellular mechanisms through which the reactive electrophile BHT-quinone methide can mediate alterations in gene expression, such as occur in tumor promotion in vivo.
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PMID:Quinone methide mediates in vitro induction of ornithine decarboxylase by the tumor promoter butylated hydroxytoluene hydroperoxide. 820 81


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