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PubMed1999

A new chemical preservative that permits analysis of urine sediment for light microscopic examination 12 h after emission.

INTRODUCTION: Urine diagnosis by light microscopy is considerably more difficult when specimens are analyzed after a certain period of time. OBJECTIVES: (1) To investigate whether this change effectively exists at a significant level of 12 h. (2) To apply measures, once the above has been done, allowing for the analysis of samples beyond 12 h in similar conditions. MATERIALS AND METHODS: Both freshly produced urine and pathological samples were used under certain experimental conditions: initial, 12 h, 12 h + fridge at 4 degrees C (F), 12 h + chemical preservation (S) and 12 h + SF. The chemical preservative was prepared at a 50/50 ratio with 3% formaldehyde and 2.5% glutaraldehyde by the addition of a buffer of pH 7.2-7.4, resulting in a solution of pH 7.35 at 25 degrees C room temperature. Urinalysis was carried out on all samples: glucose (enzymatic method of hexokinase) and total protein in liquid (red pyrogallol method). Centrifugation was followed by sediment analysis with light microscopy. Statistical analysis was done with the Kolmogorov-Smirnov normality test, Friedman nonparametric test and multiple comparisons. RESULTS AND CONCLUSION: Urine samples tested 12 h after having been produced changed significantly (p<0.0001), making it necessary to adopt certain measures to maintain their initial conditions. In our case, after the addition of the chemical preservative, samples did not present any changes (p>0.10) in relation to the initial conditions and were seen to be reliable, therefore indicating the suitability and effectiveness of the analytical conditions (urinalysis in particular, sediment analysis).

Erythrocytes↗
PubMed1996

Role of nitric oxide and its interaction with superoxide in the suppression of cardiac muscle mitochondrial respiration. Involvement in response to hypoxia/reoxygenation.

BACKGROUND: Nitric oxide (NO); superoxide anion (O2.d-); the reaction product of NO with O2.d-, peroxynitrite (ONOO-); and ischemia/reperfusion have all been reported to inhibit respiration in isolated mitochondria. However, the specific species involved in the inhibition of respiration in intact tissues are poorly understood. METHODS AND RESULTS: O2 consumption in isolated cardiac muscle from bovine calf hearts was quantified by use of a Clark-type electrode. Exogenous and endogenous sources of NO, from S-nitroso-N-acetylpenicillamine (SNAP) and bradykinin or carbachol, reversibly inhibited respiration, whereas the O2.- releasing agent, pyrogallol (PG), inhibited respiration in a manner that was only partially reversed when examined 15 minutes after the removal of PG. The generation of ONOO- with SNAP + PG caused a potentiation of the O2(-)-elicited inhibition of respiration when examined 15 minutes after the removal of the ONOO- generating system. Tiron (a scavenger of O2.-) did not alter the actions of SNAP, but it attenuated the direct inhibitory effects of PG +/- SNAP and essentially eliminated the suppression of respiration observed 15 minutes after removal of the O2.- or ONOO- generating system. Urate (a scavenger of ONOO-) antagonized only the actions of PG + SNAP. After exposure of muscle slices to a model of hypoxia (15 minutes) and reoxygenation (10 minutes), respiratory inhibition was observed. This reoxygenation-induced inhibition was potentiated by L-arginine, the substrate for NO biosynthesis, and was markedly blocked by nitro-L-arginine (an NO synthase inhibitor), Tiron, or urate. CONCLUSIONS: The potentially physiological reversible regulation of respiration in cardiac muscle by NO is converted to an effect that does not show rapid reversibility under conditions in which ONOO- forms, and this could contribute to cardiac dysfunction in situations such as hypoxia/reoxygenation.

Animals↗
PubMed1989

Rabbit polymorphonuclear neutrophils elicit endothelium-dependent contraction in vascular smooth muscle.

The present studies were designed to investigate the interaction between activated polymorphonuclear neutrophils (PMNs) and endothelial regulation of vascular smooth muscle function. Rabbit peritoneal PMNs (4 x 10(3)-4 x 10(5) cells/ml) added to muscle bath chambers containing phenylephrine-precontracted rabbit isolated aortic rings produced no effect on vascular tone. However, when PMNs were activated with the chemotactic peptide, f-met-leu-phe (0.1 microM), PMNs produced concentration-dependent vascular contraction, which was dependent on the presence of the endothelium. Aortic rings denuded of endothelium were unaffected by activated PMNs. Superoxide dismutase (100 units/ml) treatment of tissues blocked completely PMN-induced vascular contraction, whereas mannitol (20 mM) had no significant effect on PMN-induced vascular contraction. Pyrogallol (a generator of superoxide anion) produced a response that was similar to that observed with activated PMNs. Superoxide anion production was measured separately, and the time of peak rate of superoxide anion production corresponded to the time of the maximal vascular contractile responses. Activated PMNs added to vascular tissues undergoing endothelium-dependent relaxation mediated by either acetylcholine or A23187 produced a reversal of vascular relaxation. Furthermore, activated PMNs did not have any effect on endothelium-independent vascular relaxation produced by either isoproterenol or nitroglycerin. The present investigation reveals that activated PMNs can release superoxide anion and produce endothelium-dependent contraction. The endothelium-dependent contraction may be the result of superoxide anion inactivation of endothelium-derived relaxing factor.

Animals↗
PubMed1991

Role of nitric oxide and cyclic GMP as mediators of endothelium-independent neurogenic relaxation in bovine mesenteric artery.

Electrical field stimulation (EFS) of phenylephrine-contracted bovine mesenteric arteries pretreated with guanethidine elicited a relaxation that amounted to roughly 40%. This relaxation was sensitive to tetrodotoxin pretreatment, suggesting a neurogenic origin. The EFS-induced relaxation was correlated to an increase in cGMP level, from 14.2 +/- 2.5 pmol/g wet wt in nonstimulated arteries to 31.6 +/- 3.4 pmol/g wet wt after 1 minute of EFS. cAMP values were not affected by EFS. Methylene blue (5 microM) and the compound LY 83583 (10 microM), inhibitors of soluble guanylate cyclase, inhibited the EFS-induced relaxation by 60% and 50%, respectively. Zaprinast (1 microM), a selective inhibitor of cGMP degradation, significantly (p = 0.005) potentiated the EFS-induced relaxation. The relaxation induced by EFS in bovine mesenteric arteries exhibits characteristics similar to the relaxations evoked by organic nitroesters and endothelium-dependent vasodilators, both of which are suggested to be mediated by cGMP and probably with nitric oxide as the common activator of the cGMP system. The possible involvement of nitric oxide as a mediator of EFS-induced relaxations was investigated with the use of known modulators of endogenous nitric oxide production. Preincubation of the arteries with 1 mM arginine or 1 mM N-alpha-benzoyl-L-arginine, both reported to potentiate endogenous nitric oxide production, or 5 mM L-canavanine, 0.25 mM NG-monomethyl-L-arginine, or 0.1 mM NG-nitro-L-arginine, alleged inhibitors of endogenous nitric oxide production, were without effect on the relaxation induced by EFS. However, pyrogallol, a generator of superoxide anions, was a potent inhibitor of relaxations induced by EFS in bovine mesenteric arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1998

Inhibition of rat cardiac muscle contraction and mitochondrial respiration by endogenous peroxynitrite formation during posthypoxic reoxygenation.

This study was designed to investigate the potential role of endogenous peroxynitrite (ONOO-) formation in the inhibition of cardiac muscle contractility and mitochondrial respiration during posthypoxic reoxygenation. Isometric contraction of isolated rat left ventricular posterior papillary muscle was virtually eliminated at the end of an exposure to 15 minutes of hypoxia and remained 40+/-5% depressed an hour after the reintroduction of O2. O2 uptake by rat left ventricular cardiac muscle, measured by a Clark-type O2 electrode, was also inhibited by 24+/-2% at 10 minutes after reoxygenation. The inhibition of contractility and respiration during posthypoxic reoxygenation was markedly attenuated by the NO synthase inhibitor nitro-L-arginine, exogenous superoxide dismutase, and the ONOO- scavenger urate but not by the hydroxyl radical scavenger mannitol. Generation of ONOO- with the NO donor S-nitroso-N-acetylpenicillamine (SNAP) plus the superoxide-releasing agent pyrogallol caused an irreversible inhibition of cardiac contractile and respiratory function. Unlike ONOO-, exogenous (SNAP) and endogenous (bradykinin) sources of NO inhibited contractility in a reversible manner. Under conditions of comparable amounts of respiratory inhibition in unstimulated incubated muscle, the NO-dependent agents and the mitochondrial antagonist NaCN produced a smaller degree of suppression of contractility compared with ONOO- and posthypoxic reoxygenation. These results are consistent with a contributing role for endogenous ONOO- formation in the inhibition of cardiac muscle contractility and mitochondrial respiration during posthypoxic reoxygenation.

Animals↗
PubMed1991

Loss of endothelium-dependent relaxant activity in the pulmonary circulation of rats exposed to chronic hypoxia.

To determine whether exposure to chronic hypoxia and subsequent development of pulmonary hypertension induces alterations of endothelium-dependent relaxation in rat pulmonary vascular bed, we studied isolated lung preparations from rats exposed to either room air (controls) or hypoxia (H) during 1 wk (1W-H), 3 wk (3W-H), or 3W-H followed by 48 h recovery to room air (3WH + R). In lungs pretreated with meclofenamate (3 microM), the endothelium-dependent vasodilator responses to acetylcholine (10(-9)-10(-6) M) and ionophore A23187 (10(-9)-10(-7) M) were examined during conditions of increased tone by U46619 (50 pmol/min). Acetylcholine or A23187 produced dose-dependent vasodilation in control lungs, this response was reduced in group 1W-H (P less than 0.02), abolished in group 3W-H (P less than 0.001), and restored in group 3WH + R. In contrast, the endothelium-independent vasodilator agent sodium nitroprusside remained fully active in group 3W-H. The pressor response to 300 pM endothelin was greater in group 3W-H than in controls (6.8 +/- 0.5 mmHg vs. 1.6 +/- 0.2 mmHg, P less than 0.001) but was not potentiated by the endothelium-dependent relaxing factor (EDRF) antagonists: hydroquinone (10(-4) M); methylene blue (10(-4) M); and pyrogallol (3 x 10(-5) M) as it was in controls. It was similar to controls in group 3W-H + R. Our results demonstrate that hypoxia-induced pulmonary hypertension is associated with a loss of EDRF activity in pulmonary vessels, with a rapid recovery on return to a normoxic environment.

Acetylcholine↗
PubMed1999

Superoxide Anion Generation, Superoxide Dismutase Activity, and Nitric Oxide Release in Human Internal Mammary Artery and Saphenous Vein Segments.

BACKGROUND: Internal mammary artery (IMA) as conduit for a coronary artery bypass graft (CABG) stays patent longer and more often than saphenous vein (SV). However, the precise differences in the biology of IMA and SV are unclear. METHODS AND RESULTS: To examine inherent difference in superoxide anion, superoxide dismutase (SOD) and nitric oxide (NO) formation in IMA and SV as a basis for differences in patency rates, we measured these parameters in vascular segments of patients undergoing CABG. Superoxide anion generation was measured by lucigenin chemiluminescence and reduction of cytochrome c, SOD by inhibition of pyrogallol auto-oxidation, and No as nitrite/nitrate fluorometrically using 2-3-diaminonaphthalene as a probe. Generation of superoxide anion, SOD activity, and No formation were all greater in the IMA than in the SV segments (IMA:SV = 2.6:1, 2.9:1, 1, and 3.0:1, respectively, all P <.010. There was a positive correlation between superoxide anion generation and SOD activity (r = 0.65, P <.05; r = 0.70, P <.05 in IMA and SV, respectively) and NO release (r = 0.68, P <.05; r = 0.75, P <.03 in IMA and SV, respectively). Western blot analysis showed no differences in SOD and NO synthase protein expression in IMA and SV segment homogenates. To examine whether greater superoxide anion generation, SOD activity, and NO formation are unique to IMA, we studied pulmonary artery (PA) and pulmonary vein (PV) segments taken from patients undergoing lung resection. Superoxide anion generation, SOD activity, and NO formation were also found to be greater in PA than in PV segments. CONCLUSIONS: Inherently greater superoxide anion generation and subsequently increased formation of SOD and NO release in IMA (vs SV) may be a factor in the greater patency of the former as CABG conduit. Because both IMA and PA are exposed to pulsatile stretch and cary blood at higher pressure than the SV and PV, it is likely that these 2 factorsd account for the observed differences.

Journal Article↗
PubMed2004

Rubia cordifolia, Fagonia cretica linn and Tinospora cordifolia exert neuroprotection by modulating the antioxidant system in rat hippocampal slices subjected to oxygen glucose deprivation.

BACKGROUND: The major damaging factor during and after the ischemic/hypoxic insult is the generation of free radicals, which leads to apoptosis, necrosis and ultimately cell death. Rubia cordifolia (RC), Fagonia cretica linn (FC) and Tinospora cordifolia (TC) have been reported to contain a wide variety of antioxidants and have been in use in the eastern system of medicine for various disorders. However, their mechanism of action was largely unknown. We therefore selected these herbs for the present study to test their neuroprotective ability and the associated mechanism in rat hippocampal slices subjected to oxygen-glucose deprivation (OGD). METHODS: Hippocampal Slices were subjected to OGD (oxygen glucose deprivation) and divided into 3 groups: control, OGD and OGD + drug treated. Cytosolic Cu-Zn superoxide dismutase (Cu-Zn SOD), reduced glutathione (GSH), glutathione peroxidase (GPx), nitric oxide (NO) was measured as nitrite (NO2) in the supernatant and protein assays were performed in the respective groups at various time intervals. EPR was used to establish the antioxidant effect of RC, FC and TC with respect to superoxide anion (O2.-), hydroxyl radicals (. OH), nitric oxide (NO) radical and peroxynitrite anion (ONOO) generated from pyrogallol, menadione, DETA-NO and Sin-1 respectively. RT-PCR was performed for the three groups for GCLC, iNOS, Cu-Zn SOD and GAPDH gene expression. RESULTS: All the three herbs were effective in elevating the GSH levels, expression of the gamma-glutamylcysteine ligase and Cu-Zn SOD genes. The herbs also exhibited strong free radical scavenging properties against reactive oxygen and nitrogen species as studied by electron paramagnetic resonance spectroscopy. In addition all the three herbs significantly diminished the expression of iNOS gene after 48 hours which plays a major role in neuronal injury during hypoxia/ischemia. CONCLUSIONS: RC, FC and TC therefore attenuate oxidative stress mediated cell injury during OGD and exert the above effects at both the cytosolic as well as at gene expression level and may be an effective therapeutic tool against ischemic brain damage.

Animals↗
PubMed1988

Deficiency of superoxide dismutase in endemic goiter tissue.

Superoxide dismutase (SOD) activity and its concentration were measured in thyroid tissues obtained from patients with Graves' disease, Hashimoto's thyroiditis, differentiated thyroid cancer, and endemic goiter (before and after iodine supplementation) as well as in normal thyroid tissue (paranodular tissue) from patients with follicular adenomas. SOD activity was measured by pyrogallol assay in ethanol-chloroform extracts of the thyroid homogenates. The SOD concentration in the thyroid extract was measured as immunoreactive SOD by electroimmunoassay. Endemic goiter tissues (n = 10) contained significantly lower SOD activity [mean, 1.9 +/- 1.9 (+/- SD) vs. 7.5 +/- 3.9 ng purified SOD/micrograms DNA; P less than 0.02] and concentration (mean, 0.2 +/- 0.1 vs. 0.8 +/- 0.5 ng SOD/microgram DNA; P less than 0.01) compared with those of normal tissues. No other pathological thyroid tissues had such consistently low SOD levels. Lactate dehydrogenase activity, a marker of cytosolic enzyme, was not lower in endemic goiter tissues than in normal tissues, suggesting that both tissues possessed functioning cells capable of producing cytosolic enzyme. Thyroid tissue from endemic goiter patients previously treated with iodized oil injection also had low SOD activity and concentration. Western blot analysis indicated that SOD protein in the endemic goiter tissue did not differ from that in normal thyroid tissue. We conclude that there is deficiency of cytosolic SOD in endemic goiter tissue. Since the deficiency of cytosolic SOD causes more prolonged exposure to oxygen free radicals, the decrease in SOD might contribute to the degenerative changes frequently found in these tissues.

Blotting, Western↗
PubMed2004

Inhibition of P-glycoprotein function by tea catechins in KB-C2 cells.

We studied the effects of tea catechins, (-)-epicatechin (EC), (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECG), and (-)-epigallocatechin gallate (EGCG) on the P-glycoprotein (P-gp) function in multidrug-resistant P-gp over-expressing KB-C2 cells. EC did not have any effects on cellular accumulation of P-gp substrates, rhodamine-123 and daunorubicin, but the other catechins increased the accumulation in the order of EGC < ECG < EGCG. The effects of EGCG were larger than those of verapamil and quercetin. Since these catechins inhibited the efflux of P-gp substrates, the elevation of substrate accumulation seemed to be induced by the inhibition of the efflux transporter. The results showed that the inhibitory effects of the catechins did not depend on their total hydrophobicity, but significantly depended on their chemical structure. The presence of the galloyl moiety on the C-ring markedly increased the n-octanol/PBS partition coefficients of the catechins and their activity on P-gp. On the other hand, the presence of the trihydric pyrogallol group as the B-ring decreased the partition coefficients but increased the activity on P-gp, compared with the action of the corresponding catechins with a dihydric catechol B-ring.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Peripheral N-methyl-D-aspartate receptors modulate nonadrenergic noncholinergic lower esophageal sphincter relaxation in rabbits.

We investigated the role of peripheral N-methyl-D-aspartate (NMDA) receptors in the myenteric plexus in mediating nonadrenergic noncholinergic (NANC) nitrergic relaxation of the lower esophageal sphincter (LES). Isometric contraction of LES strips from Japanese White rabbits was measured. NANC relaxation was induced by KCl (30 mM) in the presence of atropine and guanethidine. The concentration of 3',5'-cyclic guanosine monophosphate (cGMP) was measured using a radioimmunoassay. The muscle strips were exposed to diethyldithiocarbamic acid (DETCA; 3 mM) to inactivate Cu/Zn superoxide dismutase. MK801 (5-methyl-10,11-dihydroxy-5H-dibenzo(a,d)cyclohepten-5,10-imine) inhibited NANC relaxation in a concentration-dependent manner (EC50 = 1.5 x 10(-5) M), accompanied by a decrease in cGMP production. NMDA induced a concentration-dependent relaxation, which was antagonized by MK801. NMDA stimulated cGMP production, which was inhibited by N(G)-nitro-L-arginine. Superoxide dismutase (100 U/mL) shifted the concentration-response relationship of MK801-mediated inhibition of NANC relaxation to the right (EC50 = 3.4 x 10(-5) M), whereas catalase did not. Treatment with DETCA shifted the concentration-response relationships of pyrogallol-, ketamine- and MK801-mediated inhibition of NANC relaxation to the left. These findings suggest that the peripheral NMDA receptors mediate NANC smooth muscle relaxation, and modulate it, in part, through extracellular production of superoxide anions, thus eliminating the relaxant effect of endogenous nitric oxide.

Animals↗
PubMed2000

Determination of alpha-tocopherol and alpha-tocopherylquinone in rat tissues and plasma by high-performance liquid chromatography with electrochemical detection.

Alpha-tocopherol and alpha-tocopherylquinone in rat tissues and plasma were determined simultaneously by using high-performance liquid chromatography-electrochemical detection (HPLC-ED) with dual electrodes in the series mode. Biological samples were saponified in the presence of a mixture of butylated hydroxytoluene, ascorbic acid, and pyrogallol and then extracted with hexane. The compounds were separated on a C18 column using a mobile phase containing 95% methanol and 0.05 M sodium perchlorate as the supporting electrolyte. After HPLC separation, alpha-tocopherylquinone was first reduced at an upstream electrode at -500 mV Both alpha-tocopherol and the reduction product of alpha-tocopherylquinone were then oxidized downstream at +600 mV. Only the downstream electrode current was monitored for the determination. Linearity of the standard curves was obtained over the range 5-30 pmol for alpha-tocopherol and alpha-tocopherylquinone. Minimum detectable quantities (S/N of 3) were 0.25 pmol for alpha-tocopherol and 0.31 pmol for alpha-tocopherylquinone. The method was applied to analysis of the contents of alpha-tocopherol and alpha-tocopherylquinone in rat tissues and plasma. By hyperoxia, the content of alpha-tocopherol was decreased remarkably in lung, and in contrast, the contents of alpha-tocopherylquinone were increased in all tissues studied with the exception of plasma, though the content of alpha-tocopherylquinone in normal rats is quite small. The technique is particularly useful in the quantitation of the oxidation of alpha-tocopherol in biological samples.

Animals↗
PubMed2002

Structural requirements of flavonoids and related compounds for aldose reductase inhibitory activity.

The methanolic extracts of several natural medicines and medicinal foodstuffs were found to show an inhibitory effect on rat lens aldose reductase. In most cases, flavonoids were isolated as the active constituents by bioassay-guided separation, and among them, quercitrin (IC(50)=0.15 microM), guaijaverin (0.18 microM), and desmanthin-1 (0.082 microM) exhibited potent inhibitory activity. Desmanthin-1 showed the most potent activity, which was equivalent to that of a commercial synthetic aldose reductase inhibitor, epalrestat (0.072 microM). In order to clarify the structural requirements of flavonoids for aldose reductase inhibitory activity, various flavonoids and related compounds were examined. The results suggested the following structural requirements of flavonoid: 1) the flavones and flavonols having the 7-hydroxyl and/or catechol moiety at the B ring (the 3',4'-dihydroxyl moiety) exhibit the strong activity; 2) the 5-hydroxyl moiety does not affect the activity; 3) the 3-hydroxyl and 7-O-glucosyl moieties reduce the activity; 4) the 2-3 double bond enhances the activity; 5) the flavones and flavonols having the catechol moiety at the B ring exhibit stronger activity than those having the pyrogallol moiety (the 3',4',5'-trihydroxyl moiety).

Aldehyde Reductase↗
PubMed2005

Non-reductive scavenging of 1,1-diphenyl-2-picrylhydrazyl (DPPH) by peroxyradical: a useful method for quantitative analysis of peroxyradical.

A stable radical 1,1-diphenyl-2-picrylhydrazyl (DPPH) has long been used as a convenient method for the antioxidant assay of biological materials such as cysteine, glutathione, ascorbic acid, tocopherol and polyhydroxy aromatic compounds (hydroquinone, pyrogallol, etc.). In this study, non-reductive scavenging of DPPH was investigated by electron spin resonance (ESR) analyses for the purpose of developing a useful method for quantitative determination of peroxyradical. Since DPPH was degraded in the presence of peroxyradical derived from UV-irradiated benzoylperoxide and the peroxyradical-induced degradation of DPPH was inhibited by the addition of a spin trapping agent 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), it is concluded that DPPH is non-reductively scavenged by peroxyradical. Therefore, it is suggested that DPPH could be a useful agent for the quantitative measurement of peroxyradical.

Biphenyl Compounds↗
PubMed2006

Studies on nepalese crude drugs. XXVIII. Chemical constituents of Bhote Khair, the underground parts of Eskemukerjea megacarpum HARA.

From the underground parts of Eskemukerjea megacarpum HARA, two new stilbenes (14, 15) were isolated, together with a known coumarin, 5,7-dihydroxycoumarin (1), a tyramine derivative, trans-feruloyltyramine (2), two pyrogallol derivatives, gallic acid (3) and beta-glucogallin (4), four flavonoids, trifolin (5), hyperin (6), myricetin 3-O-beta-D-galactopyranoside (7), and myricitrin (8), five stilbenes, resveratorol (9), astringenin (10), piceid (11) astringin (12), and resveratorol 3-O-beta-D-(6-O-galloyl)glucopyranoside (13), a flavan-3-ol, (-)-epigallocatechin 3-O-gallate (16), two proanthocyanidins, catechin-(4alpha-->8)-epigallocatechin 3-O-gallate (17) and epicatechin 3-O-gallate-(4beta-->8)-epigallocatechin 3-O-gallate (18), and an anthocyanin, idaein (19). Compounds 14 and 15 were identified as (E)-3,5,3',4'-tetrahydroxystilbene 3-O-beta-D-(6-O-galloyl)glucopyranoside and (E)-3,5,4'-trihydroxystilbene 3-O-beta-D-(6-O-galloyl)glucopyranoside, respectively, based on spectral and chemical data.

Coumarins↗
PubMed2003

Production of hydrogen peroxide by polyphenols and polyphenol-rich beverages under quasi-physiological conditions.

To investigate the ability of the production of H(2)O(2) by polyphenols, we incubated various phenolic compounds and natural polyphenols under a quasi-physiological pH and temperature (pH 7.4, 37 degrees C), and then measured the formation of H(2)O(2) by the ferrous ion oxidation-xylenol orange assay. Pyrocatechol, hydroquinone, pyrogallol, 1,2,4-benzenetriol, and polyphenols such as catechins yielded a significant amount of H(2)O(2). We also examined the effects of a metal chelator, pH, and O(2) on the H(2)O(2)-generating property, and the generation of H(2)O(2) by the polyphenol-rich beverages, green tea, black tea, and coffee, was determined. The features of the H(2)O(2)-generating property of green tea, black tea, and coffee were in good agreement with that of phenolic compounds, suggesting that polyphenols are responsible for the generation of H(2)O(2) in beverages. From the results, the possible significances of the H(2)O(2)-generating property of polyphenols for biological systems are discussed.

Antioxidants↗
PubMed2001

Nitric oxide generation in aqueous solutions of cigarette smoke and approaches to its origin.

By using the ESR spin trapping technique with the N-methyl-D-glucamine dithiocarbamate (MGD)2-Fe(II) complex, the generation of nitric oxide (NO), a gaseous free radical, was observed in NO spin trapping solution bubbled with the filtered main-stream of cigarette smoke. The ESR signal with a three-line spectrum characteristic of an NO radical, which was not observed immediately after bubbling of smoke, started rapidly increasing with time up to around 25 min after the last addition of ferrous ions Fe(II), and then slowly approached a peak value dependent on the burned cigarette mass and on the smoking speed. The production of NO was, however, much affected by air oxidation and enhanced by the addition of ascorbic acid. A certain concentration of sodium nitrite (NaNO2) solution, in which nitrite NO2- is assumed as the main origin of the NO, mimicked closely the time course of NO generation resulting from the smoke of one cigarette. The cigarette smoke that was passed through alkaline pyrogallol solution as a deoxidizer; however, it exhibited an unchanged intensity of NO signal throughout the measurement. These results strongly suggest that NO would be gradually reproduced from NO2- in the reductive aqueous solution containing excess Fe(II) through NO2, which is initially formed and is concomitantly oxidized from NO in cigarette smoke.

Antioxidants↗
PubMed2005

Novel bacterial molybdenum and tungsten enzymes: three-dimensional structure, spectroscopy, and reaction mechanism.

The molybdenum enzymes 4-hydroxybenzoyl-CoA reductase and pyrogallol-phloroglucinol transhydroxylase and the tungsten enzyme acetylene hydratase catalyze reductive dehydroxylation reactions, i.e., transhydroxylation between phenolic residues and the addition of water to a triple bond. Such activities are unusual for this class of enzymes, which carry either a mononuclear Mo or W center. Crystallization and subsequent structural analysis by high-resolution X-ray crystallography has helped to resolve the reaction centers of these enzymes to a degree that allows us to understand the interaction of the enzyme and the respective substrate(s) in detail, and to develop a concept for the respective reaction mechanism, at least in two cases.

Bacteria, Anaerobic↗