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Biomedical subjects

R Ogura

Publications and source records attributed to R Ogura.

At least 19 recordsLinked to original sources
PubMed2006

Antifungal activity of DNA-lipid complexes and DNA-lipid films against Candida species.

In this study amphiphilic lipids, DNA-lipid complexes, and DNA-lipid films were prepared, and their antifungal activity against Candida species was examined. The amphiphilic lipids were synthesized from a reaction of glycine or L-alanine with n-alkyl alcohol in the presence of p-toluene sulfonic acid. DNA-lipid complexes, which were prepared by the simple mixing of DNA and amphiphilic lipids, were insoluble in water. Self-standing, water-insoluble DNA-lipid films were prepared by casting the DNA-lipid complexes from a chloroform/ethanol solution. The antifungal activities of the lipids and DNA-lipid complexes against the Candida species were evaluated by minimum inhibitory concentrations (MICs); those of DNA-lipid films were evaluated by the disk diffusion method. The seven kinds of lipids, DNA-lipid complexes, and DNA-lipid films showed antifungal activity, and no differences were seen in the antifungal activities between glycine and L-alanine derivatives. The lipids, DNA-lipid complexes, and DNA-lipid films, which have shorter alkyl chain length in lipids, showed antifungal activity against all Candida species. However, the effect of antifungal activity against Candida species decreased with increased alkyl chain length in lipids. In this study, it was found that lipids, DNA-lipid complexes, and films with a decyl or dodecyl group exhibit more favorable antifungal activity.

Animals↗
PubMed2005

Genotoxicity studies on dietary diacylglycerol (DAG) oil.

Dietary diacylglycerol (DAG) oil is an edible oil enriched in DAG (more than 80%). A recent investigation indicated that DAG oil or its components may have beneficial effects on the prevention and management of obesity. We evaluated the genotoxic potential of DAG oil using standard genotoxicity tests. Bacterial reverse mutation assay (Ames test), the chromosomal aberration assay in cultured Chinese hamster lung cells (CHL/IU), and a bone marrow micronucleus assay in ICR CD mice were employed in the present study. In addition we have tested the possibility that genotoxic substances may be formed during cooking, heated DAG oil (HDG) was prepared by batch frying potato slices in the oil at 180 degrees C for 8 h/day for three consecutive days. Therefore, genotoxicity tests were also performed on HDG. Results obtained did not show any genotoxic effect on either unheated DAG oil (UDG) or HDG. We conclude that there are no safety concerns on the genotoxicity of DAG oil under the conditions for normal use.

Animals↗
PubMed2005

Relation between the TIMI frame count and the degree of microvascular injury after primary coronary angioplasty in patients with acute anterior myocardial infarction.

OBJECTIVE: To investigate the relation between thrombolysis in myocardial infarction (TIMI) frame count (TFC) and coronary blood flow velocity (CBFV) parameters reflecting the degree of microvascular injury in patients with acute myocardial infarction. RESULTS: TFC and CBFV were measured after primary coronary angioplasty in 103 consecutive patients with their first anterior wall acute myocardial infarction. TFC correlated inversely with the averaged peak velocity (r = -0.43, p < 0.0001). However, TFC did not correlate significantly with diastolic deceleration time and with the averaged systolic peak velocity (r = -0.16, p = 0.22, and r = -0.23, p = 0.16, respectively). The patients were divided into two groups according to presence (35 patients) or absence (68 patients) of systolic flow reversal. There was no significant difference in TFC between the two groups (29 (16) v 25 (13), p = 0.20). CONCLUSIONS: These findings suggest that the TFC reflects epicardial CBFV. However, it is not accurate enough to assess the degree of microvascular injury after primary coronary angioplasty.

Aged↗
PubMed1995

Properties of Ca(2+)-dependent K+ channels of human gingival fibroblasts.

Cells in the oral cavity are normally exposed to different temperatures. Ion transport systems are influenced by temperature in other tissues: In particular, changes in intracellular K+ ion can affect cell growth and synthesis of macromolecules. The purpose of this investigation was to identify K+ channels in human gingival fibroblast cells and analyze the effect of temperature on their K+ conduction properties. Ca(2+)-dependent K+ channels with a large conductance (125 pS in symmetrical K(+)-rich solutions) were identified in human gingival fibroblasts and studied by the patch-clamp technique. The open probability of the channels varied with membrane potential between +40 and -100 mV. When the bath temperature was decreased from 40 to 4 degrees C, channel conductance was reduced, but the mean open time of the channels was increased. The activation energies for the conductance and the reciprocal of the mean open time were estimated to be 9.1 and 22.9 kJ/mol, respectively. These values are lower than those reported for these and other types of channels in cells from other tissues. The open probability of the channels was nearly constant in the temperature range studied. These results suggest that the properties of Ca(2+)-dependent K+ channels of gingival fibroblasts remain relatively unchanged when the cells are exposed to a wide range of temperatures.

Body Temperature↗
PubMed1993

Effect of alpha-tocopherol on high energy phosphate metabolite levels in rat heart by 31P-NMR using a Langendorff perfusion technique.

To examine the action of alpha-tocopherol on high energy phosphate compounds, a 31P-NMR technique was applied to perfused Langendorff rat hearts. Rats were treated with tocopherol acetate (25 mg/kg body wt i.p.) for 7 consecutive days. On the 7th day, the rat hearts were isolated for the Langendorff experiment. After 30 min of global ischemia the NMR signals of creatine phosphate and ATP in myocardium disappeared, and then recovered slightly in the reperfusion following ischemia. However, in the tocopherol-treated rat hearts, the restoration of high energy phosphate compounds occurred quickly after the beginning of reperfusion, although there was no significant difference in the destruction of high energy phosphate compounds during the ischemia. The alpha-tocopherol level in the myocardium was severely depleted by ischemia-reperfusion. In the alpha-tocopherol-treated animals, the alpha-tocopherol level in myocardium was still significantly higher than the control level at the end of 30 min of global ischemia. The heart mitochondrial respiratory function was simultaneously protected against ischemia-reperfusion injury. The role of alpha-tocopherol was discussed as a radical scavenger and membrane stabilizer against oxygen stress.

Adenine Nucleotides↗
PubMed1993

Hydroxyl radical generation and membrane fluidity of erythrocytes treated with lipopolysaccharide.

The effect of lipopolysaccharide (LPS) and/or bile acids on rat erythrocyte membranes was studied in vitro. Addition of LPS isolated from E. coli (J5 mutant) into the erythrocyte resulted in the decrease of membrane fluidity as determined by spin labelling using electron paramagnetic resonance (EPR). This was accompanied by membrane fragility. It was found that hydroxyl radicals were generated from erythrocytes treated with LPS by using DMPO spin trapping. However, pretreatment of erythrocytes with taurine-conjugated bile acids was found to modify the membrane response induced by LPS. Taurocholic acid (TCA) and tauroursodeoxycholic acid (TUDCA) prevented the decrease of membrane fluidity induced by LPS, and, as a result, the membrane integrity was maintained although no significant changes were observed in the amount of hydroxyl radicals produced by LPS addition. However, taurochenodeoxycholic acid (TCDCA) exhibited little beneficial effect on the dynamic properties and the function of the erythrocyte membranes, although the hydroxyl radical declined markedly in the erythrocytes. Therefore, it is suggested that TCA and TUDCA have a protective effect against LPS-induced membrane fragility by modulating membrane fluidity.

Animals↗
PubMed1992

Effect of vitamin E on cytotoxicity, DNA single strand breaks, chromosomal aberrations, and mutation in Chinese hamster V-79 cells exposed to ultraviolet-B light.

The effect of pretreatment with vitamin E on cytotoxicity, DNA single strand breaks, and chromosomal aberrations as well as on mutation induced by ultraviolet-B light (UV-B) was investigated in Chinese hamster V-79 cells. Cellular pretreatment with non-toxic levels of 25 microM alpha-tocopherol succinate (vitamin E) for 24 h prior to exposure resulted in a 10-fold increase in cellular levels of alpha-tocopherol. Using a colony-forming assay, this pretreatment decreased the cytotoxicity of UV-B light. However, alkaline elution assays demonstrated that pretreatment with vitamin E did not affect the number of DNA single strand breaks caused by UV-B light. In addition, UV-B exposure produced a dose-dependent induction of chromosomal aberrations and mutations at the HGPRT locus, and neither of these actions of UV-B was influenced by pretreatment with the vitamin. These results suggest that vitamin E protects cells from UV-B-induced cytotoxicity, possibly through its ability to scavenge free radicals. The results also suggest that the extent of genotoxicity induced by UV-B light may not correlate directly with the cytotoxic action of this wavelength region in sunlight.

Animals↗
PubMed1992

Fatal encephalitis/encephalopathy in primary human herpesvirus-6 infection.

An encephalitic illness with a fatal outcome occurred in a 9 month old girl with virologically confirmed exanthem subitum. Human herpes-virus-6 (HHV-6) DNA was found in the cerebrospinal fluid at the acute stage of the disease by the polymerase chain reaction, but the virus antigen was not detected in her brain tissue. This suggests that HHV-6-induced encephalitis/encephalopathy may be due to a non-infectious process.

Antigens, Viral↗
PubMed1992

Identification of free and esterified hydroxyoctadecadienoates (HODEs) and linoleate-hydroxylating pathway in the epidermis of hairless mice.

Epidermal homogenates of hairless mice contained a large amount of lipid material showing a single peak on reverse phase (RP)-high pressure liquid chromatography (HPLC) with a maximum absorbance of 234 nm, which was different in retention time from arachidonate metabolites such as 12-HETE, 15-HETE and 5-HETE. The production of this material was dependent on exogenous linoleate concentration, protein concentration and buffer pH. This material was identified to be a mixture of 13-HODE and 9-HODE on the basis of UV absorbance spectra, retention times on RP-HPLC, straight phase (SP)-HPLC, gas chromatography-mass spectrometry (GC/MS) and mass spectra obtained. As assessed by SP-HPLC after saponification, these two HODEs were found to exist primarily in esterified forms in the skin. Neither substance was produced following heat denaturation of the homogenate. These results indicate that 13- and 9-HODEs are produced from linoleate enzymatically at physiologically relevant levels in the epidermis of hairless mice. Thus, it is possible that these two materials may play some important role in pathophysiology of the skin.

Animals↗
PubMed1992

Hydroxyl radical generation from heart mitochondria damaged by ischemia.

The hydroxyl radicals are known to be a biologically active oxygen species. A remarkable enhancement of hydroxyl radical generation was observed in the mitochondria obtained from ischemic myocardium. The hydroxyl radicals are the primary reactive species leading to cellular damages, such as membrane damages, DNA damages, enzyme inactivation, protein denaturation and so forth. The origin of the hydroxyl radicals appeared in mitochondria was discussed.

Animals↗
PubMed1991

Electron spin resonance studies on the mechanism of adriamycin-induced heart mitochondrial damages.

Rats were given i.p. injections of Adriamycin (4 mg/kg body weight) for 6 consecutive days. Electron spin resonance spectrometry with spin labeling and a trapping technique was applied to heart mitochondria obtained from treated and control animals, in order to examine the physical response of heart mitochondrial membrane affected by Adriamycin. The Adriamycin treatment resulted in a decrease of membrane fluidity (and an increase in order parameter S), with concomitant dysfunction of respiratory responses. The generation of hydroxyl radicals from mitochondria was enhanced in the Adriamycin-treated group. In addition, superoxide dismutase activity in the mitochondrial matrix was found to decrease. The heart mitochondria of Adriamycin-treated animals contained a large amount of lipid peroxide. These results suggest that the enhancement of hydroxyl radical formation in mitochondria affected by Adriamycin is one of the factors involved in Adriamycin-induced cardiotoxicity.

Animals↗
PubMed1991

Effect of ascorbic acid on DNA damage, cytotoxicity, glutathione reductase, and formation of paramagnetic chromium in Chinese hamster V-79 cells treated with sodium chromate(VI).

The effect of pretreatment with ascorbic acid (vitamin C) on chromate-induced DNA damage, cytotoxicity, and enzyme inhibition as well as on the cellular reduction of chromium(VI) was investigated using Chinese hamster V-79 cells. Cellular pretreatment with nontoxic levels of 1 mM ascorbic acid for 24 h prior to exposure resulted in a significant increase (1.7-fold) in cellular levels of this vitamin. Alkaline elution assays demonstrated that this pretreatment decreased cellular levels of Na2CrO4-induced alkali-labile sites while the numbers of DNA-protein crosslinks produced by chromate increased. In colony-forming assays, pretreatment with ascorbic acid enhanced the cytotoxicity of chromate. However, the inhibition of glutathione reductase attributed to Na2CrO4 was attenuated by this pretreatment. Under the same experimental condition, the uptake of chromate in pretreated cells was found to increase. ESR studies revealed that cellular pretreatment with ascorbic acid reduced the level of chromium(V) intermediate and increased the level of chromium(III) complex, indicating that cellular reduction of chromium(VI) to chromium(III) was accelerated by this vitamin. These results suggest that ascorbic acid decreases chromate-induced alkali-labile sites and chromium inhibition of glutathione reductase, but it enhances DNA-protein cross-links and cytotoxicity caused by this metal through its ability to directly reduce chromium(VI).

Animals↗
PubMed1991

Reduction of chromium(VI) in Chinese hamster V-79 cells.

The cellular reduction of chromate(VI) was studied by electron spin resonance spectrometry. Incubation of Chinese hamster V-79 cells with Na2CrO4 resulted in the formation of both chromium(V) and chromium(III) complex in a manner dependent on time (30 min-2 h) and concentration (50-500 microM). Following removal of extracellular chromate, the level of chromium(V) complex decreased quickly during the first hour but more slowly for the next hour, whereas the level of chromium(III) remained unchanged, indicating that chromium(III) is the ultimate ion of this metal in cells. Alkaline elution studies demonstrated that treatment of cells with Na2CrO4 induced DNA single-strand breaks that decreased quickly and DNA-protein crosslinks that persisted for 2 h after removal of this metal. These results suggest that the cellular levels of chromium(V) and chromium(III) may be associated with the formation of DNA damage induced by chromium (VI).

Animals↗
PubMed1991

Prevention of 4-pentenoic acid-induced liver injury in rats by 16,16-dimethyl PGE2.

16,16-Dimethyl PGE2 (dmPGE2) is known to protect against cellular damage in various tissues. Histological and biochemical approaches were used to examine the effect of this prostaglandin on hepatocellular damage in an experimental Reye's syndrome model produced in rats by 4-pentenoic acid. Chronic intraperitoneal administration of 4-pentenoic acid induced an accumulation of fatty droplets throughout the hepatic lobules along with mitochondrial abnormalities including swelling, disappearance of christae, and heterogeneity of matrix. These abnormalities were more intense in the marginal zone and successively decreased nearer to the central vein. Such hepatic abnormalities were markedly reduced by the combined administration of dmPGE2 with 4-pentenoic acid. Biochemical examination confirmed that dmPGE2 was able to inhibit the accumulation of hepatic triglyceride seen after the treatment with 4-pentenoic acid alone. These results indicated that dmPGE2 can prevent characteristic hepatocellular damage in this experimental Reye's syndrome model, suggesting that the involvement of prostaglandins should be taken into account in discussing the etiology and management of this syndrome.

16,16-Dimethylprostaglandin E2↗
PubMed1991

Generation of leukotrienes and hydroxyeicosatetraenoic acids in peritoneal macrophages of tumor-bearing mice.

To examine the potential role of lipoxygenase products in the pathophysiology observed after experimental tumor implantation, we examined the generation of leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs) in peritoneal macrophages. C57BL/6 mice were given subcutaneous inoculations of B16 melanoma cells, and peritoneal macrophages were isolated various days after the inoculation. Macrophages were incubated for 1 h at 37 degrees C in serum-free RPM11640 containing 10 microM calcium ionophore A23187, 10 microM exogenous arachidonic acid (AA), 5 mM cysteine hydrochloride and 1 mM reduced glutathione. LTs and HETEs were separately extracted, passed through Sep-Pak cartridges, then identified and quantitated with a HPLC system using UV absorbance. The B16 melanoma-cell-treated/untreated macrophages were found to produce substantial amounts of 15-HETE, 12-HETE and 5-HETE and LTC4 by enzymatic mechanisms. Thus, when determined under various conditions, the production of HETEs was dependent on substrate-concentration, incubation-time and cell-number. The production of LTC4 was dependent on incubation-time and cell number but not substrate-concentration, indicating utilization of endogenous AA stores. Of these products, 12-HETE and LTC4 showed a significant increase on the fourth day after the tumor cell inoculation and returned to the control level by the 11th day after the same treatment. These results suggest that in vivo tumor cell implantation may induce a transient increase of 12-HETE and LTC4 production in macrophages.

Animals↗
PubMed1991

Involvement of active oxygen in lipid peroxide radical reaction of epidermal homogenate following ultraviolet light exposure.

To elucidate the radical mechanism of lipid peroxidation induced by ultraviolet light (UV) irradiation, an electron spin resonance (ESR) study was made on epidermal homogenate prepared from albino rat skin. The exposure of the homogenate to UV light resulted in an increase in lipid peroxide content, which was proportional to the time of UV exposure. Using ESR spin trapping (dimethyl-1-pyrroline-N-oxide, DMPO), the DMPO spin adduct spectrum of lipid radicals (L.) was measured following UV exposure (DMPO-L.:aN = 15.5 G, aH = 22.7 G), as was the spectrum of DMPO-hydroxyl radical (DMPO-OH, aN = aH = 15.5 G). In the presence of superoxide dismutase, the DMPO spin adduct spectrum of lipid radicals was found to be reduced remarkably. Therefore, it was shown that the generation of the lipid radicals partially involves superoxide anion radicals, in addition to hydroxyl radicals. In the ESR free-radical experiment, an ESR signal appeared at g = 2.0064 when the ESR tube filled with homogenate was exposed to UV light at -150 degrees C. The temperature-dependent change in the ESR free radical signal of homogenate exposed to UV light was observed at temperatures varying from -150 degrees C to room temperature. By using degassed samples, it was confirmed that oxygen is involved in the formation of the lipid peroxide radicals (LOO.) from the lipid radicals (L.).

Animals↗
PubMed1991

Mechanism of lipid radical formation following exposure of epidermal homogenate to ultraviolet light.

It has been suggested that oxygen free radicals are important mediators of lipid peroxidation in the epidermis exposed to ultraviolet (UV) light. However, it is not clear whether it is the superoxide anion radical (O2-.) or the hydroxyl radical (.OH) that plays the major role in producing the lipid radicals (L.) following UV exposure. In this study, we used electron spin resonance (ESR) technique with the spin trap (5,5-dimethyl-1-pyrroline-N-oxide [DMPO]) to determine which active oxygen species is involved in the UV-induced lipid radical formation (DMPO-L.: aN = 15.5 G, aH = 22.7 G). In the presence of superoxide dismutase or the metal-chelating agent, the DMPO-spin adduct spectrum of lipid radicals was reduced remarkably. The lipid radicals were formed by the hydroxyl radical generation system, not the superoxide anion generation system. The hydroxyl radical was found to be the direct active oxygen species that can generate lipid radicals as a result of .OH-mediated hydrogen atom abstraction. Superoxide anion radical stimulated the generation of hydroxyl radical via the iron-catalyzed reaction.

Animals↗