Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Several aspects of intestinal function and morphology are affected by acute radiation damage, including changes in the activity of proliferative cells in the crypts, immune cell populations, and the transport of various substrates. This study was designed to compare the time course of the recovery of intestinal proliferation, transport, and leukocyte population following radiation injury. Rats received a single dose of 6 Gy to the abdomen from a 137Cs source and were studied 3, 7, and 14 days later. No changes in the passive uptake of L-glucose or D-leucine were observed in the jejunum. Active transport of D-glucose and maximal water uptake were reduced at 3 days but had returned to normal by 7 days, whereas L-leucine uptake required more than 7 days to return to control levels. Mucosal permeability, assessed by an in vivo potential difference technique, remained increased 7 days after irradiation. Ornithine decarboxylase, an indicator of DNA synthetic activity, was elevated following radiation treatment and remained so even after 14 days. By comparison, myeloperoxidase activity, used as a quantitative monitor of granulocyte numbers, was still reduced after 7 days. These data indicate that while certain parameters of gut function may return to normal soon after radiation injury, the recovery of other factors is more prolonged. Thus the return of transport function to normal values post irradiation may be viewed as an adaptive change rather than simply the recovery of the tissue.
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PMID:The assessment of recovery of the intestine after acute radiation injury. 302 42

Sunscreen preparations are evaluated according to their protection against biological effects of ultraviolet radiation. UV-induced phenomena found on protected skin are compared with those on unprotected skin; thus the sunprotection factor is estimated. In order to assess the photoprotective power of sunscreens, only early UV-induced effects are decisive - such as erythema. PUVA erythema, pigmentation, activation of the ornithine decarboxylase, the influence on Langerhans cells, appearance of 'sunburn' cells, and changes of the DNA metabolism. We report on the various methods to obtain the specific sunprotection factors against UVB and UVA. Water-resistance, photostability, and pharmacokinetics depending on the vehicle are further criteria with regard to the evaluation of sunscreens. We rely on consumers information regarding the following properties of sunscreens: stickness, oily shine, greasiness, discoloration, odor, and tolerance.
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PMID:[Evaluation of sunscreening agents]. 305 7

Sunscreen preparations are evaluated according to their protection power against biological effects of ultraviolet radiation. UV-induced phenomena found on protected skin are compared with those on unprotected skin; thus the sunprotection factor is estimated. In order to assess the photoprotective power of sunscreens, only early UV-induced effects are decisive--such as erythema. PUVA erythema, pigmentation, activation of the ornithine decarboxylase, the influence on Langerhans cells, appearance of 'sunburn' cells, and changes of the DNA metabolism. We report on the various methods to obtain the specific sunprotection factors against UVB and UVA. Water-resistance, photostability, and pharmacokinetics depending on the vehicle are further criteria with regard to the evaluation of sunscreens. We rely on consumers information regarding the following properties of sunscreens: stickiness, oily shine, greasiness, discoloration, odor, and tolerance.
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PMID:[Evaluation of sunscreening agents]. 306 67

alpha-Difluoromethylornithine (DFMO), an enzyme-activated irreversible inhibitor of ornithine decarboxylase, was used alone and in combination with multiple doses of methylglyoxal-bis(guanylhydrazone) (MGBG) to treat mice with systemic L1210 leukemia. Used as a single agent (administered p.o. as a 3% solution in tap water), DFMO exerted a weak therapeutic effect against this tumor. The therapeutic effect of MGBG (administered i.p. at 50 mg/kg/day) was only slightly better. However, 1-3 days of pretreatment with DFMO strongly potentiated the effect of MGBG treatment. Thus, mice treated with the combination exhibited an increase in life span of up to 138%. The prolonged survival of leukemic mice treated with a combination of DFMO and MGBG was associated with inhibition of polyamine synthesis and a marked decrease in the spermidine and spermine content of the tumor cells as compared to untreated controls. As a consequence, there was a continuous decrease in the S- and G2-phase fractions with a concomitant increase in G1. Used singly, DFMO and MGBG had no significant effect on the cell-cycle distribution. The effects of the combination of DFMO and MGBG on the cell-cycle distribution are consistent with the contention that polyamine deficiency primarily interferes with initiation of DNA synthesis. However, the possibility that selective S-phase kill partly contributes to this change in cell-cycle distribution cannot be excluded.
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PMID:Synergistic antileukemic effect of two polyamine synthesis inhibitors. Host survival and cell-cycle kinetic analysis. 308 54

In vivo effects of DL-alpha-difluoromethylornithine (DFMO) on the metabolism of polyamines and nucleotide phosphates were monitored in P388/S leukemia cells grown intraperitoneally in BDF1 inbred male mice. Inhibiting the ornithine decarboxylase (ODC) activity DFMO depleted putrescine and spermidine to 30-50 and 50-60%, respectively, and increased spermine to 25-60% compared with the controls, when given as 2% solution in drinking water of the tumor-bearing animals. DFMO treatment caused a parallel 56% elevation of total nucleotide content in tumor cells with distinct and significant increase of some nucleotide phosphates. The most pronounced alterations were shown in the intracellular UTP (202%), CTP (103%), ADP (92%) and ATP (71%) concentrations. Changes in polyamine and nucleotide phosphate metabolisms were dependent on tumor progression. A possible explanation of the metabolic events induced by DFMO is discussed.
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PMID:In vivo effects of DL-alpha-difluoromethylornithine on the polyamine and nucleotide phosphate metabolism in P388/S leukemia cells. 308 89

The effect of combined treatment with D,L-2-difluoromethylornithine (DFMO) and tamoxifen on the growth status, ornithine decarboxylase (ODC) activity and polyamine content of established 1-methyl-1-nitrosourea (MNU)-induced mammary tumors was investigated. DFMO treatment, a 0.125% solution provided as drinking water, inhibited the rate of tumor occurrence and reduced the number of mammary tumors induced by a high dose of MNU (50 mg/kg body weight) during the first 120 days post-carcinogen treatment. Tamoxifen was administered daily via s.c. injection (25 micrograms/100 g body weight) to tumor-bearing rats in both treatment groups, i.e. control and DFMO-treated, for a 30-day period beginning 120 days after carcinogen. Tamoxifen treatment induced tumor regression but the percentage of regressing, static or growing tumors was no different in the presence or absence of DFMO. Whereas the mammary tumors of DFMO-treated rats had reduced ODC activity and lower polyamine concentrations in comparison to the tumors of untreated animals, tamoxifen had no effect on these parameters independent of its effect on tumor growth status. DFMO did not increase the efficacy of tamoxifen in inducing tumor regression.
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PMID:Effect of tamoxifen and D,L-2-difluoromethylornithine on the growth, ornithine decarboxylase activity and polyamine content of mammary carcinomas induced by 1-methyl-1-nitrosourea. 308 21

The effects of dietary supplementation of 13-cis-retinoic acid (13-cis-RA) and alpha-difluoromethylornithine (DFMO) in the drinking water on 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted skin tumor formation was determined. Administration of 13-cis-RA in the diet and DFMO in the drinking water was started 1 week and 2 days before the first TPA application to the dimethylbenz[a]anthracene-initiated skin of either female CD-1 or SENCAR mice, respectively. Dietary 13-cis-RA failed to inhibit both the tumor yield and the incidence; papillomas per mouse at 0, 5, 50, 100 and 200 mg/kg diet 13-cis-RA doses were 25, 30, 22, 28 and 25 respectively at 18 weeks of promotion treatment and at all doses 100% of the mice bore papillomas. However, dietary 13-cis-RA dramatically reduced the size of skin tumor promoted with TPA. 13-Cis-RA at doses of 5, 50, 100 and 200 mg/kg diet inhibited skin papillomas (greater than 4 mm diameter) per mouse by 28, 55, 76 and 93%, respectively. Retinoid treatment did not affect body weight gains and the survival was more than 80% in all groups. In accord with our previous findings, DFMO when given in drinking water, was a very effective inhibitor of mouse skin tumor promotion by TPA; DFMO at 0.25% concentration inhibited the number of papillomas by 50%. Inhibition of skin tumor promotion by combined treatments with dietary 13-cis-RA (100 mg/kg) and DFMO (0.25%) in the drinking water was possibly additive. The retinoid and DFMO preclude TPA-increased ornithine decarboxylase (ODC) activity and the accumulation of putrescine by differential effects on ODC, an enzyme associated with skin tumor promotion by TPA.
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PMID:Modulation of mouse skin tumor promotion by dietary 13-cis-retinoic acid and alpha-difluoromethylornithine. 308 64

The purpose of this study was to examine the role of ornithine decarboxylase (ODC) in the stimulation of the growth of gastrointestinal mucosa following feeding. Rats were divided into five groups: 1) fasted for 2 days, 2) fasted for 2 days and refed for 2 days, 3) fasted for 2 days and refed with the addition of 5% difluoromethylornithine (DFMO) to the drinking water, 4) normally fed, and 5) normally fed plus 5% DFMO in the drinking water. In general the results show a significant dissociation between ODC activity and growth of gastrointestinal mucosa in response to feeding. In the gastric mucosa, growth was inhibited by fasting and DFMO and stimulated by feeding, but there were no significant changes in ODC activity in any of the five groups. In the ileum ODC activity increased dramatically in refed rats and was essentially eliminated in rats fed DFMO. DFMO, however, had no effect on mucosal growth in fed rats and only prevented part of the trophic response to refeeding. The results in the colon were much the same as in the ileum, except that DFMO prevented even less of the trophic response to refeeding, despite total inhibition of ODC. These data suggest that polyamines necessary for growth of gastrointestinal mucosa following feeding are not supplied by the rapid activation of mucosal ornithine decarboxylase.
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PMID:Ornithine decarboxylase and mucosal growth in response to feeding. 309 Aug 96

The objective of this study was to evaluate induction of ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis, and subsequent polyamine accumulation in interleukin-2 (IL-2)- and interleukin-3 (IL-3)-dependent growth. The CTLL-20 and FDC-P1 cell lines, which have been shown to be absolutely dependent on IL-2 and IL-3, respectively, were used in these studies. The CTLL-20 and FDC-P1 cells each had different temporal patterns of ODC induction following lymphokine stimulation. ODC levels increased rapidly in the FDC-P1 cells, peaking 4 hr after stimulation with IL-3. In contrast, peak ODC activity in the CTLL-20 cells occurred 18 hr following stimulation with IL-2 and reached eightfold higher levels than those observed in the FDC-P1 cells. Treatment with D,L-alpha-difluoromethylornithine X HCl X H2O (DFMO), a specific irreversible inhibitor of ODC activity, completely abrogated lymphokine-dependent ODC induction in both the CTLL-20 and FDC-P1 cell lines. Similarly, intracellular levels of the polyamines putrescine and spermidine were reduced in both cell lines following DFMO treatment. DFMO treatment reduced both IL-2- and IL-3-dependent proliferation in a dose-dependent manner. However, this inhibition could be reversed by the addition of exogenous putrescine. DFMO treatment had no effect on cell viability. Polyamine-depleted CTLL-20 and FDC-P1 cells showed decreased absorption of IL-2 and IL-3 activity, respectively. However, the addition of exogenous putrescine restored the ability of the cells to absorb the appropriate lymphokine. These data are the first to demonstrate that ODC induction and polyamine biosynthesis are required in lymphokine dependent growth.
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PMID:Ornithine decarboxylase induction and polyamine biosynthesis are required for the growth of interleukin-2- and interleukin-3-dependent cell lines. 309 95

The purpose of this investigation was to establish an efficient route and dose regime for the long-term administration of tamoxifen in the study of mammary tumorigenesis in the rat. The second objective of this work was to determine whether treatment with D,L-2-difluoromethylornithine (DFMO), a synthetic inhibitor of the enzyme ornithine decarboxylase, would reduce the occurrence of mammary cancers in tamoxifen-treated or ovariectomized rats. A total of 265 female Sprague-Dawley rats were assigned to one of two experimental protocols. All animals were injected with 50 mg 1-methyl-1-nitrosourea (MNU) per kg body wt at 50 days of age. In experiment 1, beginning 7 days after the injection of the carcinogen, animals were assigned to one of six groups which received either 0, 1 or 5 mg tamoxifen citrate per kg AIN-76A purified diet in addition to either no DFMO or a 0.125% w/v solution of DFMO as the drinking water. The experiment was terminated 180 days following carcinogen treatment. Treatment with tamoxifen resulted in a dose-dependent reduction in cancer incidence, and the number of cancers induced and significantly prolonged the median cancer-free time. This effect was also accompanied by a decrease in the rate of body weight gain. Treatment with DFMO delayed latency and reduced tumor number. DFMO in addition to tamoxifen (1 mg/kg diet) further prolonged latency. In experiment 2 each animal was assigned to one or four treatment groups when its first palpable mammary tumor was detected. At that time each was either ovariectomized or sham-operated. In addition, the rats were either provided no DFMO or a 0.5% w/v solution of DFMO as the drinking water. The study was terminated 35 weeks following carcinogen injection. Ovariectomy significantly inhibited the occurrence of additional mammary tumors. Ovariectomy plus DFMO was more effective than ovariectomy alone in reducing tumor number. Collectively, these observations indicate that suppression of polyamine biosynthesis via the systemic administration of DFMO inhibits the development of ovarian hormone insensitive mammary tumors.
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PMID:Effect of D,L-2-difluoromethylornithine and endocrine manipulation on the induction of mammary carcinogenesis by 1-methyl-1-nitrosourea. 309 87


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