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)

Green tea, next to water, is the most popular and commonly consumed beverage in the world, especially in eastern countries. In prior studies we have shown that the polyphenolic fraction isolated from green tea (GTP) exerts antigenotoxic effects in various mutagenicity test systems (Mutat. Res., 223: 273-285, 1989) and that its topical application or oral feeding in drinking water protects against polycyclic aromatic hydrocarbon-induced skin tumor initiation and complete carcinogenesis in SENCAR and BALB/c mice [Cancer Lett., 42: 7-12, 1988; Carcinogenesis (Lond.), 10: 411-415, 1989] and UV B radiation-induced photocarcinogenesis in SKH-1 hairless mice [Carcinogenesis (Lond.), 12: 1527-1530, 1991]. In the present study we assessed the effect of skin application of GTP to SENCAR mice on 12-O-tetradecanoylphorbol-13-acetate (TPA) and other skin tumor promoter-caused induction of epidermal ornithine decarboxylase (ODC) activity. Topical application of GTP to mouse skin inhibited TPA-induced epidermal ODC activity in a dose-dependent manner. The inhibitory effect of GTP was also dependent on the time of its application relative to TPA treatment. Maximum inhibitory effect was observed when GTP was applied 30 min prior to topical application of TPA. GTP application to animals also inhibited the induction of epidermal ODC activity caused by several structurally different mouse skin tumor promoters. In order to identify which of the specific epicatechin derivatives present in GTP is responsible for these inhibitory effects, they were isolated from GTP and evaluated for their inhibitory effects against TPA-caused induction of epidermal ODC activity. Among these, (-)epigallocatechin-3-gallate (EGCG), which was the major constituent present in GTP by weight, exerted the maximum inhibition. EGCG also showed greater inhibitory effects against TPA-caused induction of epidermal ODC activity when compared with several other naturally occurring polyphenols. The results of this study suggest that GTP, specifically its epicatechin derivative EGCG, could provide anti-tumor-promoting effects against a wide spectrum of skin tumor promoters.
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PMID:Inhibition of skin tumor promoter-caused induction of epidermal ornithine decarboxylase in SENCAR mice by polyphenolic fraction isolated from green tea and its individual epicatechin derivatives. 161 28

The dorsal skin of hairless mice (Skh:HR-1) was treated with multiple applications of acetone, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or ethyl phenylpropionate (EPP) two times per week, or exposed to ultraviolet radiation (UVR) three times per week for treatment periods up to 16 weeks. Epidermal hyperplasia, as measured by epidermal thickness, was increased in all three treatment groups after a single (0.5 weeks) TPA, EPP, or UVR treatment. TPA- and EPP-induced hyperplasia had begun to subside by 16 weeks, whereas UVR-induced hyperplasia was still increasing at that point. Epidermal homogenates were examined for ornithine decarboxylase (ODC) activity 6 h after the final treatment at 0.5, 2, 8, and 16 weeks of treatment. ODC activity was elevated in all treatment groups (TPA greater than EPP greater than UVR), with UVR induction returning to near control (acetone) levels by 16 weeks even though the UVR-induced hyperplasia continued to increase at the 16-week point. Homogenates examined for superoxide dismutase (SOD), catalase (CAT), and xanthine oxidase (XO) activity 48 h after the final treatment at 0.5, 2, 4, 8, 12, and 16 weeks had decreased activities of both SOD and CAT. TPA and EPP elevated XO, but UVR had little or no effect. Our data indicate that promoter-induced hyperplasia persists for extended periods of time and that diminution of antioxidant defenses observed following prolonged tumor-promoter treatment persists through the time period when tumors would be expected to begin. This antioxidant diminution may be one of a cascade of events that leads to epidermal proliferation and tumor promotion in mouse skin.
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PMID:Effects of multiple applications of tumor promoters and ultraviolet radiation on epidermal proliferation and antioxidant status. 162 31

The influence of topical PUVA on the activity of ornithine decarboxylase (ODC) and its gene expression was investigated in the skin of hairless mouse. After 1 h of application of 0.3% 8-methoxypsoralen, irradiation of 3 J/cm2 of ultraviolet A (UV-A) was administered. The ODC activity markedly increased and peaked at 24 h following UV-A irradiation. The ODC mRNA level, analyzed in dot-blot analysis, elevated to about 5 times that of control at 24 h after treatment. These results show that the PUVA-induced ODC activity is due in part to an increase in ODC gene expression.
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PMID:PUVA increases ornithine decarboxylase gene expression in mouse skin. 170 4

In the treatment of various dermatological disorders, topically applied retinoids have potential therapeutic use with the advantage of improved localized activity and lower toxicity over systemically administered retinoids. However, most retinoids cause a significant degree of local irritation. In the present study, the ability to produce local activity with low local irritation potential was evaluated with a novel retinoic acid derivative. BMY 30047 (11-cis, 13-cis-12-hydroxymethylretinoic acid delta-lactone) is one of a series of retinoic acid derivatives in which the carboxyl function of the polar end was modified with the aim of achieving reduced local irritation and systemic toxicity while retaining the local therapeutic effect. BMY 30047 was evaluated and compared with all-trans retinoic acid for topical retinoid activity in several preclinical assay systems, including the utricle reduction assay in rhino mice, 12-o-tetradecanoylphorbol 13-acetate ester-stimulated ornithine decarboxylase induction in hairless mice and the UV light-induced photodamaged skin model in hairless mice. BMY 30047 was assessed for retinoid-type side effects by evaluating the skin irritation potential in rabbits after repeated topical application, and hypervitaminosis A-inducing potential in mice after i.p. injection. BMY 30047 demonstrated significant topical retinoid activity in several in vivo models with less skin irritation potential relative to the most used clinical concentrations of all-trans retinoic acid. BMY 30047 also showed very little systemic activity and did not produce any evidence of hypervitaminosis A syndrome at systemic doses 20 times greater than the no-effect dose of all-trans retinoic acid.
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PMID:BMY 30047: a novel topically active retinoid with low local and systemic toxicity. 198 66

Epidermal hyperplasia was induced in hairless mice (hr/hr) by topical n-hexadecane treatment of tail and back skin. Following this skin irritation, a granular layer developed in interfollicular regions of the tail epidermis. An increase of ornithine decarboxylase activity, of thymidine triphosphate incorporation into DNA and of amino acid incorporation into protein was found. Shown histologically and by measurement of the called biochemical parameters, ciclosporin (cyclosporin A, CAS 59865-13-3; pretreatment with 30 mg/kg b.w. per day subcutaneously for 7 days) inhibited the development of epidermal hyperplasia in back and tail epidermis.
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PMID:Inhibition of n-hexadecane-induced epidermal hyperplasia due to systemically administered ciclosporin. 204 75

The inhibitory effect of cyclosporine A (CsA) on the activity of ornithine decarboxylase (ODC) induced by phorbol ester tumor promoter has been reported. In the present study, the effects of CsA on ODC activity induced by ultraviolet-B (UV-B) and PUVA in the skin of the SKH/hr 1 hairless mouse were investigated. Topical application of CsA (1.7 mumol) to the dorsal skin irradiated with 50 mJ/cm2 UV-B did not remarkably change ODC activity. On the other hand, if CsA was applied simultaneously with 3 J/cm2 UV-A 1 h after treatment with 0.3% 8-methoxypsoralen, PUVA-induced ODC activity was suppressed by about 60% at 12 and 24 h after UV-A irradiation. In the dot blotting analysis of ODC-specific mRNA level, a significant but slight decrease in ODC mRNA level (about 20% inhibition) was observed in the PUVA-treated group compared with the control group (vehicle and UV-A). The inhibition of PUVA-induced ODC activity by CsA may have been caused in part by the decrease in ODC mRNA level and in part by a post-transcriptional regulation mechanism.
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PMID:Differential effects of cyclosporine A on ornithine decarboxylase activity induced by ultraviolet-B and PUVA in mouse skin. 204 75

The cellular effects of u.v. radiation have been studied by using a hairless-mouse model in vivo. U.v. B radiation (u.v.B) induced the activity of the enzyme ornithine decarboxylase (ODC) in mouse epidermis. Maximal induction was noted after radiation with 90 mJ/cm2, and increased ODC activity was first detected 2 h after u.v.B exposure. U.v.B. also induced the expression of the ODC gene in a time- and dose-dependent manner, but did not induce the levels of actin mRNA transcripts. Cycloheximide treatment did not alter basal levels of ODC mRNA transcripts and had no effect on the u.v.B induction of ODC-gene expression. The results of these experiments demonstrate that u.v.B radiation induces both the expression of the ODC gene and the activity of the enzyme, and provides a useful 'in vivo' paradigm for the analysis of the molecular effects of u.v.B radiation.
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PMID:Ultraviolet B radiation induction of ornithine decarboxylase gene expression in mouse epidermis. 224 91

The effects of acute, multiple, and chronic exposure of hairless mice to ultraviolet radiation (UVR) on induction of epidermal ornithine decarboxylase (ODC) (EC 4.1.1.17) activity were investigated. Acute UVR exposure results in a biphasic time course of induction of epidermal ODC activity. Enzyme activity maxima occur at 3 and 24 h postirradiation. The biphasic time course is observed in two different strains of hairless mice (Skh:HR-1 and Jackson HRS/J) when the UVR source is either UBV fluorescent tubes or a solar simulator. The ratio of 24-h/3-h postirradiation ODC activity increases with increasing UVR dose. UVR induction of ODC activity was not significant below the mouse minimum erythemal dose (MED). The 3- and 24-h ODC activities have similar apparent Kms for ornithine (34 and 50 microM, respectively), and thermal stabilities at 52 degrees C (t1/2 = 23 and 18 min, respectively), and exhibit similar half-lives in vivo (t1/2 = 15 and 18 min, respectively). Multiple UVR exposure experiments showed 24-h ODC activity is sensitive to the preexposure history of the mouse, while 3-h ODC is not. Preexposure of hairless mice to several sub-MED levels of simulated solar radiation (SSR) specifically suppresses induction of 24-h ODC by a follow-up 2 x MED of SSR. Preexposure to a single 2 x MED of SSR specifically enhances induction of 24-h ODC induced by a second 2 x MED of SSR administered 48 h after the first. The 3-h ODC was not significantly affected by either preexposure regimen. Preexposure to a single high or low dose of UVA radiation did not affect epidermal ODC activity nor had an effect on ODC induction by UVB radiation. Several weeks of chronic exposure to UVB radiation elevated basal levels of epidermal ODC substantially (up to 350-fold). In these chronically irradiated mice, exposure to 2 x MED SSR resulted in a further 3.5-fold increase in ODC activity over the elevated basal level. These data reveal novel properties of epidermal cell expression of ODC activity in response to acute and chronic UVR insult. The results provide additional insight into the use of ODC as a marker for skin photodamage.
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PMID:Acute and chronic ultraviolet radiation induction of epidermal ornithine decarboxylase activity in hairless mice. 230 17

The effects of a single exposure to UVB radiation on skin antioxidant enzymes and superoxide-generating xanthine oxidase were examined in Skh:HR-1 hairless mice. Significant decreases in superoxide dismutase (SOD) and catalase (CAT) were observed by 12 h after UV irradiation and remained depressed for up to 72 h. No induction of xanthine dehydrogenase (XD) or xanthine oxidase (XO) occurred with UV treatment, although significant hyperplasia was evident. Ornithine decarboxylase was induced after UV irradiation as has been previously reported. These results demonstrate significant biochemical effects of a single dose of UVB on murine epidermis, especially in terms of antioxidant defenses.
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PMID:Effects of single-dose ultraviolet radiation on skin superoxide dismutase, catalase, and xanthine oxidase in hairless mice. 238 May 80

Psoralen photochemotherapy (PUVA) is widely used in the treatment of psoriasis. Some therapy regimen have been associated with increased risk of skin cancer. Free radical species are thought to play a role in psoralen phototoxicity and photocarcinogenesis. It has been reported that the antioxidant butylated hydroxytoluene (BHT) inhibits acute phototoxicity by PUVA but does not reduce therapeutic efficacy. It has also been shown that BHT inhibits UVB-induced erythema, tumorigenesis and induction of ornithine decarboxylase (ODC) activity--ODC activity is thought by some to be associated with tumor promotion. Therefore, we have investigated the effect of BHT on psoralen tumorigenesis and PUVA-induced epidermal ODC activity. SKH-Hr-1 hairless albino mice were treated with topically applied 8-MOP and exposed to UVA (3X weekly) for 31 weeks with and without BHT administered either in the diet or topically. Induction of ODC activity was determined in similar experimental groups 24 h after a single exposure to UVA. Neither route of BHT administration had any effect on 8-MOP phototumorigenesis. However, BHT when administered in the diet reduced induction of ODC activity by 40% (p less than 0.05). These data indicate different mechanisms for UVB- and PUVA-induced carcinogenesis and again bring into question the relationship between induction of ODC activity and photocarcinogenesis.
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PMID:Effects of butylated hydroxytoluene upon PUVA-tumorigenesis and induction of ornithine decarboxylase activity in the mouse. 249 83


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