Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
J Invest Dermatol 1992 Aug
PMID:Effects of multiple applications of tumor promoters and ultraviolet radiation on epidermal proliferation and antioxidant status. 162 31

The effects of cepharanthin on inflammatory parameters such as neutrophil chemotaxis, phagocytosis and reactive oxygen species (ROS) generation, were examined. Cepharanthin significantly decreased the levels of O2-, H2O2, and OH. generated by neutrophils. H2O2 and OH. generated in a cell-free, xanthine-xanthine oxidase system were also reduced in the presence of cepharanthin. However, the drug did not affect neutrophil chemotaxis or phagocytosis. The present study indicates that cepharanthin is an effective ROS scavenger, exerting its anti-inflammatory action by reducing the potent ROS species excessively generated in tissues and organs, especially at the sites of inflammation.
J Dermatol 1991 Nov
PMID:Effects of cepharanthin on neutrophil chemotaxis, phagocytosis, and reactive oxygen species generation. 180 May 30

Comedonal bacteria, Propionibacterium acnes, P. granulosum and coagulase-negative staphylococci (CNS) seem to play an important initiating role in the inflammatory process by producing neutrophil chemotactic factors. The attracted neutrophils, after phagocytosis, release inflammatory factors such as reactive oxygen species (ROS). We investigated the effects of minocycline at subminimal inhibitory concentrations (sub-MIC), i.e. one-tenth MIC, on the production of human neutrophil chemotactic factors in comedonal bacteria, and on several inflammatory parameters of neutrophils, including neutrophil phagocytosis and generation of ROS (O2-, H2O2, OH.). ROS generation in a cell-free, xanthine-xanthine oxidase system was also assessed. Production of neutrophil chemotactic factors in all strains of P. acnes, P. granulosum and CNS were significantly suppressed by sub-MIC minocycline. Sub-MIC minocycline effectively reduced three kinds of neutrophil-generated ROS (O2-, H2O2, OH.). However, neutrophil phagocytosis and the ROS generated in a cell-free system were not markedly changed in the presence of sub-MIC minocycline. The results suggest that sub-MIC minocycline has an anti-inflammatory effect by inhibiting the production of neutrophil chemotactic factors in comedonal bacteria as well as ROS generated by neutrophils in the inflammatory process of acne.
Arch Dermatol Res 1991
PMID:Effects of subminimal inhibitory concentrations of minocycline on neutrophil chemotactic factor production in comedonal bacteria, neutrophil phagocytosis and oxygen metabolism. 183 72

On the basis of recent reports that the proportion of linoleic acid (C18:2Cis 9,12), a free fatty acid, is markedly decreased in acne comedones and that tetracycline is effective against acne comedones by acting directly as an antioxidant on infiltrating neutrophils, we investigated the effect of linoleic acid on several inflammatory parameters of neutrophils, including neutrophil chemotaxis, phagocytosis, and generation of reactive oxygen species (ROS). Linoleic acid significantly decreased phagocytosis and the generation of O2-, H2O2, and OH.by neutrophils, whereas it did not significantly inhibit neutrophil chemotaxis or decrease the ROS levels generated in a cell-free, xanthine-xanthine oxidase system. The present study seems to suggest that decreased levels of linoleic acid in acne comedones contribute, in part, to the worsening of acne inflammation by the failure of low levels of linoleic acid to suppress neutrophil phagocytosis and ROS generation.
J Invest Dermatol 1990 Sep
PMID:Suppressive effects of linoleic acid on neutrophil oxygen metabolism and phagocytosis. 214 21

Metronidazole is clinically effective in treating not only rosacea but also acne inflammation. Yet it is generally considered not to be very effective in inhibiting the growth of anaerobic Propionibacterium acnes. We report here our investigation into the synergistic effects of metronidazole and palmitoleic acid on the anaerobic growth of P. acnes as well as on human neutrophil functions, including the generation of reactive oxygen species (ROS). Both metronidazole and palmitoleic acid, when used alone, only slightly inhibited the growth of P. acnes, and no significant decrease in human neutrophil functions, including the generation of ROS, was observed. But metronidazole used in the presence of palmitoleic acid markedly inhibited the anaerobic growth of P. acnes and decreased ROS generation by neutrophils. However, ROS generated in the xanthine-xanthine oxidase system were not affected. Metronidazole was shown to be clinically effective by decreasing neutrophil-generated ROS at the sites of inflammation with the aid of palmitoleic acid, which is generally present in human skin. By inhibiting oxidative tissue injury under in vivo conditions, treatment with metronidazole results in remarkable improvement of rosacea and acne.
Arch Dermatol Res 1990
PMID:The inhibition of free radical generation by human neutrophils through the synergistic effects of metronidazole with palmitoleic acid: a possible mechanism of action of metronidazole in rosacea and acne. 215 Mar 1

Superoxide dismutase (SOD) activity in cow snout epidermis was determined by the method of electron spin resonance (ESR) using the 5, 5 dimethyl-1-pyrroline-N-oxide (DMPO) spin trapping agent. The procedure was found to be a reliable measurement as compared with the ordinary method using xanthine oxidase NBT. SOD activity was distributed through the whole epidermis. This activity was higher in the lower layer than in the upper and middle layers.
J Invest Dermatol 1990 Feb
PMID:Distribution of superoxide dismutase activity in the epidermis: measurement with electron spin resonance spin trapping. 215 33

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.
J Invest Dermatol 1990 Aug
PMID:Effects of single-dose ultraviolet radiation on skin superoxide dismutase, catalase, and xanthine oxidase in hairless mice. 238 May 80

The distributions of xanthine dehydrogenase (XD) and xanthine oxidase (XO) in subpopulations of murine keratinocytes differing in their stages of terminal differentiation were determined by enzymatic analyses. Keratinocytes were isolated from the skins of female SENCAR mice that had been treated 72 h earlier with either acetone or 12-O-tetradecanoylphorbol-13-acetate (TPA). The ratio of XO/(XD + XO) specific activities was used as an index of the XD to XO conversion. The XO/(XD + XO) ratios for basal cell, suprabasal cell, granular cell plus squamae, and horny sheet preparations isolated from acetone- or TPA-treated mice were 0.35, 0.35, 0.45, 0.75 and 0.28, 0.29, 0.58, and 1.0, respectively. Total XD + XO and XO specific activities in each subpopulation derived from TPA-treated mice were approximately twice the values measured in their control counterparts. Suspension culturing of basal cell keratinocytes in methylcellulose induced terminal differentiation and a conversion of XD to XO. The kinetics of keratin disulfide crosslinking and the XD to XO conversion were similar and preceded cornification. Collectively, these studies demonstrate that the conversion of XD to XO occurs primarily during the later stages of keratinocyte terminal differentiation. Furthermore, the increases in XO activity measured in epidermal homogenates after TPA treatment are due to TPA-dependent increases in 1) the relative proportions of keratinocytes undergoing differentiation, 2) tissue XD content, and 3) increased conversion of XD to XO.
J Invest Dermatol 1989 Jul
PMID:Conversion of xanthine dehydrogenase to xanthine oxidase occurs during keratinocyte differentiation: modulation by 12-O-tetradecanoylphorbol-13-acetate. 247 35

UVB irradiation augmented the beta-adrenergic adenylate cyclase response of pig skin epidermis in vitro. The effect was observed 2-4 h following the irradiation and lasted at least for 48 h. There was no significant difference in cyclic AMP phosphodiesterase activity between control and UVB-irradiated epidermis at lower irradiation dose (150 mJ/cm2), which is the dose of the most marked beta-adrenergic augmentation effect. The augmentation effect was specific to the beta-adrenergic system; adenosine and histamine adenylate cyclase responses were unchanged or decreased depending on the irradiation dose. Histologically, marked sunburn-cell formation was observed following the UVB irradiation. It has been suggested that oxygen intermediates generated by ultraviolet radiation participate in sunburn-cell formation. The addition of superoxide dismutase (SOD) in the incubation medium significantly inhibited sunburn-cell formation. On the other hand, the beta-adrenergic augmentation effect was not affected by the addition of SOD. Other scavengers of oxygen intermediates (catalase, catalase + SOD, xanthine, or mannitol) did not inhibit the UVB-induced beta-adrenergic augmentation effect. Further, superoxide-anion generating systems (hypoxanthine-xanthine oxidase system and acetaldehyde-xanthine oxidase system) revealed no stimulatory effect on the beta-adrenergic response of epidermis. These results indicate that (a) the UVB-induced beta-adrenergic augmentation effect is inherent to skin and does not depend on systemic factors such as inflammatory infiltrates following UVB irradiation; (b) in contrast to sunburn-cell formation, induction of the beta-adrenergic adenylate cyclase response is not directly associated with oxygen intermediates generated by UVB irradiation.
Arch Dermatol Res 1988
PMID:Effects of UVB irradiation on epidermal adenylate cyclase responses in vitro: its relation to sunburn cell formation. 289 32

To elucidate the mechanism of action of metronidazole in the treatment of rosacea, the effect of metronidazole on the generation of reactive oxygen species was examined both in neutrophil and xanthine-xanthine oxidase systems. Metronidazole had anti-oxidant action which was not exerted by the scavenging of reactive oxygen species, but by having an effect on neutrophil cell functions. Beneficial effects of metronidazole in the treatment of papulopustular rosacea can in part be attributable to this anti-inflammatory effect.
Br J Dermatol 1986 Feb
PMID:Anti-oxidant action of metronidazole: a possible mechanism of action in rosacea. 293 72


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