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At least 109 records · Page 6Linked to original sources

PubMed1978

The influence of an extraneuronal compartment on the relaxation of the cat nictitating membrane in vivo.

1 Contractions of the cat nictitating membrane were elicited on stimulation of the internal carotid nerve, and the effects were studied of desipramine and two inhibitors of catechol-O-methyltransferase, U-0521 and pyrogallol, on the subsequent relaxation of the muscle. 2 The relaxation of the nictitating membrane occurred in at least two phases. The late phase of relaxation was prolonged after increase in the period of nerve stimulation and the duration of this phase was further prolonged after treatment with pyrogallol. 3 After inhibition of neuronal uptake of noradrenaline with desipramine both the early and late phases of relaxation were increased in duration, and subsequent administration of pyrogallol or U-0521 caused a further increase in the duration of the late phase of relaxation. 4 The results suggest that the late phase of relaxation of the nictitating membrane is influenced by efflux of noradrenaline from an extraneuronal pool.

Animals↗

PubMed1987

Metabolism of gallate and phloroglucinol in Eubacterium oxidoreducens via 3-hydroxy-5-oxohexanoate.

The pathway for the anaerobic catabolism of gallic acid by Eubacterium oxidoreducans was studied by using both in vivo and cell-free systems. Cells grown with gallate and crotonate, but with no formate or H2, excreted pyrogallol and phloroglucinol into the medium. Gallate was decarboxylated by crude cell extracts, with pyrogallol as the only detectable product. Whole cells converted pyrogallol to phloroglucinol. A phloroglucinol reductase catalyzed the conversion of phloroglucinol to dihydrophloroglucinol when NADPH was used as the source of electrons. Both formate dehydrogenase (EC 1.2.1.43) and hydrogenase (EC 1.18.99.1) were present in cell extracts of gallate-formate-grown cells. These two enzymes were both NADP linked. Since either H2 or formate is required for cell growth with gallate or phloroglucinol, these results suggest that the oxidation of the reduced substrate may be indirectly linked to the reduction of phloroglucinol. A dihydrophloroglucinol hydrolase was present, which hydrolyzed dihydrophloroglucinol to 3-hydroxy-5-oxohexanoate. This six-carbon ring cleavage product then presumably can be broken down by a series of reactions similar to beta-oxidation. These reactions cleaved the six-carbon acid to 3-hydroxybutyryl-coenzyme A yielding acetate and butyrate as end products. A number of key enzymes involved in beta-oxidation and substrate-level phosphorylation were demonstrated in cell extracts.

Caproates↗

PubMed1993

Cu/Zn superoxide dismutase activity does not parallel copper levels in copper supplemented HL-60 cells.

The objective of this research was to develop a method for measuring Cu/Zn-superoxide dismutase (Cu/Zn-SOD) (E.C. 1.15.1.1) in HL-60 cells and subsequently examine the relationship between cellular copper levels and the activity of this copper-requiring enzyme. In cells such as the neutrophil or HL-60 promyelocyte cell line, the activity of Cu/Zn-SOD cannot be measured because of an increase in the oxidation rate of the substrate by some unknown compound in the cells. Others have utilized heat treatment to inactivate the responsible compounds, however, we found that heat treatment of HL-60 cells resulted in a loss of over half of the activity of the enzyme. The method described here utilizes sodium azide to inhibit the substance(s) that are responsible for the enhanced rate of pyrogallol's oxidation. Gel filtration data confirmed that the compound responsible for the enhanced rate of pyrogallol oxidation was sensitive to azide and did not affect Cu/Zn-SOD activity. When HL-60 cells were incubated with various levels of copper, Cu/Zn-SOD activity did not reflect the cellular copper levels.

Azides↗

PubMed1987

On the role of O-methylation in the metabolism of S-adenosylmethionine in rat brain.

The effects of tropolone and pyrogallol in areas of the rat brain with a high and low density of catecholaminergic innervation, i.e. the striatum and cortex, on S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) concentrations were studied and related to the extent of catechol-O-methyltransferase (COMT) inhibition. Moreover, the effects of drugs enhancing dopamine (DA) or noradrenaline (NA) utilization in these areas were also investigated. Pyrogallol reduced the concentrations of SAM in a similar manner in both areas and increased SAH much more in the cortex than in the striatum; these effects corresponded to that on O-methylation in terms of dose-effect relationships, indicating that there is no compartmentation of SAM with respect to the methylation process in which it is used. Tropolone increased SAM and decreased SAH in the striatum only, and these effects occurred at somewhat higher doses than the inhibition of COMT. Together with the data showing that DA antagonists decrease SAM in the striatum, this suggests that a significant proportion of SAM metabolism in this area results from O-methylation of DA (or its deaminated metabolite). A number of antidepressants did not alter the levels of SAM in either area, but some of the drugs increased SAH in the cortex. However, this was not correlated with their effects on the noradrenergic system. Inhibition of the synthesis and decarboxylation of SAM by cycloleucine and methylglyoxal bis(guanylhydrazone) (MGBG), respectively, did not cause the expected pattern of changes, i.e. decreases of both SAM and SAH in the former case and either increase or no change in both parameters in the latter. Instead, both cycloleucine and MGBG increased SAH while decreasing SAM, suggesting an involvement of other properties of these drugs.

Animals↗

PubMed1977

Oxygen-dependent chemical tumorigenesis in a Nicotiana hybrid: inhibition by ascorbic acid and dinitrophenol.

Aqueous solutions of molecular oxygen, per se, or in combination with either pyrogallol or 6-azauracil increased tumorigenesis in Nicotiana suaveolens X Nicotiana langsdorffii seedlings relative to control seedlings. The biological activities of the organic chemicals were O2-dependent, because the substitution of N2 or O2 or the degassing of 0.1-1 mM solutions of the compounds eliminated or greatly reduced their tumorigenic effects. Rates of tumorigenesis exceeded 95% for 0.5 mM solutions of either pyrogallol or 6-azauracil solutions in the presence of l mM O2. Although tumors developed in 20% of seedlings in the presence of 1 mM O2, alone, 4-5 times more tumors were induced by the organic chemical--O2-H2O systems. Dinitrophenol and ascorbic acid, compounds which affect cellular respiration or redox systems, strongly inhibited the chemically-mediated tumorigenesis. Dinitrophenol was equally effective at one-tenth of the molar concentrations of ascorbic acid that were required for the suppressions of oncogenesis. Dehydroascorbic acid was much less inhibitory than ascorbic acid.

Ascorbic Acid↗

PubMed1994

Pharmacological similarity between nitric oxide and the nitrergic neurotransmitter in the canine ileocolonic junction.

In organ bath experiments, pyrogallol (30-100 microM), and to a lesser extent L-cysteine (3 microM), reduced nitric oxide (NO)-induced relaxation, but not the NO-mediated non-adrenergic non-cholinergic (NANC) relaxation elicited by field stimulation of the canine ileocolonic junction. In contrast, in a superfusion bioassay, pyrogallol (10-30 microM) and L-cysteine (1 microM) inhibited the biological activity of both the transferable nitrergic factor released from the canine ileocolonic junction in response to NANC nerve stimulation and NO, but not that of S-nitroso-L-cysteine, S-nitrosoglutathione or S-nitroso-N-acetyl-D,L-penicillamine. Based on the bioassay experiments, it is concluded that the nitrergic NANC neurotransmitter in the canine ileocolonic junction behaves pharmacologically like NO.

Animals↗

PubMed1994

NANC neurotransmission in the bovine retractor penis muscle is blocked by superoxide anion following inhibition of superoxide dismutase with diethyldithiocarbamate.

This study examined the effects of inhibiting Cu/Zn superoxide dismutase with diethyldithiocarbamate (DETCA) on the ability of superoxide generating agents such as pyrogallol, hypoxanthine/xanthine oxidase and LY 83583, to influence NANC relaxation of strips of bovine retractor penis (BRP) muscle. Although pyrogallol (100 microM) and hypoxanthine (0.3 mM)/xanthine oxidase (64 mU ml-1) had little effect on NANC relaxation in control strips, both induced almost complete inhibition following treatment with DETCA (3 mM) for 1 h. Inhibition was due to the actions of superoxide anion since it was blocked by the addition of exogenous superoxide dismutase (250 U ml-1). LY 83583 (0.1-30 microM) produced a concentration-dependent inhibition of NANC relaxation even in control strips and this too was blocked by exogenous superoxide dismutase, but sensitivity to inhibition was enhanced 10-fold following treatment with DETCA. The data suggest that under normal circumstances the NANC neurotransmitter is protected by high levels of tissue superoxide dismutase, and inhibition of this enzyme increases its susceptibility to destruction by superoxide anions. An important impediment to accepting free nitric oxide as the NANC neurotransmitter in the BRP on the basis that superoxide anion-generating agents inhibit the actions of authentic nitric oxide but not those of NANC nerve stimulation has thus been removed.

Aminoquinolines↗

PubMed1992

Dipyridamole inhibits platelet aggregation induced by oxygen-derived free radicals.

Pyrogallol (a generator of superoxide anions) caused 50% increase in platelet aggregation induced by 400 microM of arachidonic acid. Dipyridamole did not produce a statistically significant inhibition of arachidonic-acid induced platelet aggregation, but it caused 100% inhibition of pyrogallol-stimulated platelet aggregation. Ferrous salts (Fe2+) induced 34% platelet aggregation which was inhibited (79.6%) by a concentration of dipyridamole of 10 microM. Dipyridamole inhibited ferrous-induced lipid peroxidation with IC-50 values of 17.5 microM. When arachidonic acid was used as aggregating agent, the corresponding IC-50 value was 140.5 microM. These results indicate that dipyridamole prevented platelet activation induced by oxygen-derived free radicals.

Adult↗

PubMed1976

Cocarcinogenic and tumor-promoting agents in tobacco carcinogenesis.

A series of 21 tobacco smoke components and related compounds werere applied to mouse skin (50 female ICR/Ha Swiss mice/group) three times weekly with a low dose (5 mug/application) of benzo[a]pyrene (B[a]P). The test compounds were of five classes: aliphatic hydrocarbons, aromatic hydrocarbons, phenols, and long-chain acids and alcohols. The following compounds enhanced remarkably the carcinogenicity of B[a]P: catechol, pyrogallol, decane, undecane, pyrene, benzo[e]pyrene, and fluoranthene. The following compounds inhibited B[a]P carcinogenicity completely: esculin, quercetin, squalene, and oleic acid. Phenol, eugenol, resorcinol, hydroquinone, hexadecane, and limonene partially inhibited B[a]P carcinogenicity. Six of the 21 compounds were also tested as tumor promoters im two-stage carcinogenesis. No direct correlation existed between tumor-promoting activity and cocarcinogenic activity. The cocarcinogens pyrogallol and catechol did not show tumor-promoting activity. Decane, tetradecane, anthralin, and phorbol myristate acetate showed both types of activity. Structure-activity relationships and possible modes of action were described.

Acids↗

PubMed1995

Enhancing and inhibitory effects of nitric oxide on superoxide anion generation in human polymorphonuclear leukocytes.

1. The effects of sodium nitroprusside (SNP, a nitric oxide donor) and authentic nitric oxide (NO) on superoxide anion (O2-) generation were investigated in human polymorphonuclear leukocytes (PMNs). 2. Neither SNP (10 nM to 10 microM) nor NO (40 nM to 40 microM) alone induced O2- generation or change of intracellular Ca2+ concentration ([Ca2+]i) in human PMNs. 3. Pretreatment with SNP or NO at the concentrations used (SNP, 10 nM to 10 microM: NO, 40 nM to 40 microM) showed a biphasic concentration-dependent effect on O2- generation induced by f-methionyl-leucyl-phenylalanine (FMLP). Low concentrations of SNP (10 nM to 100 nM) and NO (400 nM) did not affect either basal cyclic GMP levels or cyclic GMP levels stimulated by FMLP, but enhanced FMLP-induced O2- generation and [Ca2+]i elevation. On the other hand, high concentrations of SNP (10 microM) and NO (40 microM) alone elevated cyclic GMP levels and inhibited FMLP-induced O2- generation and [Ca2+]i elevation. 4. 8-Bromo-cyclic GMP (8-Br-cyclic GMP) at concentrations ranging from 1 microM to 1 mM did not induce O2- generation on its own and had little effect on FMLP-induced O2- generation and [Ca2+]i elevation. 5. Addition of a high concentration of NO (40 microM) decreased authentic O2- formation by pyrogallol in a cell-free system, but a low concentration of NO (400 nM) had no effect on this. On the other hand, addition of SNP in the concentration-ranges used had no effect on authentic O2- formation by pyrogallol. 6. In this study, we have shown that SNP and NO have dual effects (enhancement and inhibition) on 02- generation induced by FMLP in human peripheral PMNs. The results suggest that the enhancement observed with SNP and NO at low concentrations is not mediated by activation of the guanylate cyclase-cyclic GMP pathway. The suppressive effect of SNP and NO at higher concentrations is mediated by the NO-induced O2--scavenging effect and activation of the guanylate cyclase-cyclic GMP pathway.

Calcium↗

PubMed1975

Accumulation of norepinephrine (NE) by rat organs in vivo.

In anesthetized rats intravenously infused, norepinephrine (NE) was accumulated by the heart, the spleen and the lung in a dose-related manner. With the lower dose of NE (2.5 mg/kg) the organ/blood ratios were more than unity and were generally greater than with higher doses (5 and 10 mg/kg), indicating that accumulation occurred by active uptake. Nialamide and pyrogallol treatment increased accumulation in the three organs. In animals receiving nialamide and pyrogallol treatment, normetanephrine (uptake2 inhibitor) and desmethylimipramine (uptake1 inhibitor) inhibited accumulation in all the organs and the entire accumulation of NE could be ascribed to uptake1 and uptake2 processes. In these animals, phenoxybenzamine and bilateral adrenalectomy inhibited and enhanced, respectively, the accumulation in the heart and the spleen only. NE accumulated in hearts of animals in vivo could be partly washed out by perfusion with NE-free medium in vitro. Washout was prevented by normetanephrine, indicating that this effect was not a passive diffusional leakage.

Adrenal Glands↗

PubMed1985

A simple method for evaluating platelet superoxide dismutase.

A simple and rapid spectrophotometric method for evaluating platelet superoxide dismutase is reported. Platelets prepared avoiding erythrocyte and leucocyte contamination were lysated and tested in a Tris-cacodylic buffer containing pyrogallol. Platelet superoxide dismutase was calculated by evaluating the degree of the pyrogallol autoxidation inhibition induced by platelet lysate. Possible interferences of hydrogen peroxide, peroxidases and reducing substances were excluded. Platelet superoxide dismutase content was studied in 38 healthy subjects and was 19.1 +/- 4.1 U/10(8) platelets or 35 +/- 7.8 U/mg protein.

Adolescent↗

PubMed1991

Pharmacological evidence that captopril possesses an endothelium-mediated component of vasodilation: effect of sulfhydryl groups on endothelium-derived relaxing factor.

Captopril, an angiotensin-converting enzyme inhibitor, reportedly can scavenge superoxide anion (O2-), a property attributed to its sulfhydryl group. The present investigation, using rabbit aortic rings precontracted with either norepinephrine or clonidine, was designed to determine whether captopril possesses an endothelium-dependent component of vasodilation related to its ability to protect endothelium-derived relaxing factor (EDRF) from superoxide-mediated destruction. Also studied were enalaprilat, a nonsulfhydryl angiotensin-converting enzyme-inhibitor, superoxide dismutase, and the sulfhydryl compounds glutathione (GSH), N-2-mercaptopropionylglycine (MPG) and N-acetylcysteine (NAC). Captopril, but not enalaprilat, caused dose-dependent relaxations in preconstricted aortic rings containing an intact endothelium. Rings denuded of endothelium were unresponsive to any dose of captopril. Captopril's vasodilation was not related to prostaglandin influence but was associated with an increase in cyclic GMP. Superoxide dismutase, GSH, MPG and NAC also produced endothelium-dependent relaxations similar to captopril. It was also demonstrated that endothelium-dependent relaxations to acetylcholine were enhanced by captopril, GSH, MPG and NAC but not by enalaprilat. In another set of experiments, the ability of captopril to inhibit superoxide-mediated inactivation of EDRF was examined. Pyrogallol, a potent generator of O2-, and superoxide dismutase, a scavenger of O2-, were used as a basis for comparing a possible scavenging effect of captopril. In preconstricted rings, pyrogallol elicited endothelium-dependent contractions that were attenuated by both captopril and superoxide dismutase. Similar effects were found with GSH, MPG and NAC but not with enalaprilat. These results suggest that captopril's endothelium-dependent vasodilation is due to its sulfhydryl group and the ability of the latter to scavenge O2-, thereby protecting EDRF.

Acetylcholine↗

PubMed1989

Screening for microalbuminuria by use of a rapid, low-cost colorimetric assay.

We evaluated the pyrogallol red-molybdate(IV) method for quantification of urinary protein as a screening procedure for microalbuminuria by determining the assay's sensitivity and specificity at different concentrations of urinary albumin as measured by a comparison laser-nephelometric immunoassay. The pyrogallol red-molybdate(IV) method has sensitivity and specificity similar to that for other semiquantitative assays, but it is less expensive and sample throughput can be high if microtiter plate techniques are used.

Albuminuria↗

PubMed1987

Enzymatic oxidation of unconjugated bilirubin to assess its interactions with taurocholate.

The rate of peroxidation of unconjugated bilirubin (UCB), catalyzed by horseradish peroxidase (HRP), has been employed by Jacobsen (1969. FEBS Lett. 5: 112-114) to assess the fraction of unbound UCB in the presence of serum albumin. We used this method to examine the interactions of UCB with taurocholate (TC) at pH 8.2, assuming solubilization of UCB by TC is due to pigment binding and/or to partitioning into the micelle, thus rendering UCB unavailable for peroxidation. Inhibition of UCB peroxidation conformed with predictions based on these assumptions and demonstrated significant interaction of UCB with both monomeric and micellar TC. Although significant inhibition of UCB peroxidation was seen with TC monomer, inhibition was even greater with TC micelles. In contrast, pyrogallol, another substrate of HRP, acted very differently in the presence of TC. Inhibition of pyrogallol peroxidation by TC was much less than with UCB and occurred primarily with monomeric TC, with little further inhibition in the micellar range. The results of this study suggest that at taurocholate concentrations above 50 mM, similar to the physiologic bile salt concentrations in human bile, at least 99% of UCB is bound to bile salt, dramatically decreasing the concentration of unbound UCB. Since bile salts also bind Ca2+, they play a dual role in protection against the precipitation of calcium bilirubinate from bile. Therefore, bile salts are a major factor in the prevention of the formation and growth of pigment gallstones.

Bilirubin↗

PubMed1976

The actions of ketamine on vascular smooth muscle.

The responses of rabbit aortic strips superfused with noradrenaline, adrenaline and 5-HT were studied alone and in combination with ketamine (50 mug/ml). Ketamine caused a slight depression of the isolated aorta but potentiated responses to adrenaline but not to noradrenaline or 5-hydroxytryptamine. Ketamine did not potentiate aortic strips contracted to a stable level by pyrogallol and adrenaline. Experiments carried out with COMT from homogenates of rat liver showed that, in contrast to pyrogallol (10(-5) M), ketamine (10(-3) M) did not inhibit the enzyme. Other experiments with rabbits given 6-hydroxydopamine showed that aortas of these rabbits responded in a similar manner to controls when treated with ketamine and catecholamines. Results obtained with aortas contracted by adrenaline and noradrenaline with ketamine present, followed by oil immersion, showed that ketamine prolonged greatly the relaxation induced by adrenaline and to a lesser extent the relaxation induced by noradrenaline. The results of these studies indicate that ketamine prevented catecholamines from reaching the intracellular site of COMT. In this respect, ketamine can be termed an inhibitor of uptake site 2. If this hypothesis is valid then the action of ketamine on vascular tissue might explain the cardiovascular effects of the drug in man and experimental animals.

Animals↗

PubMed1990

Quantitative, standardized assays for determining the concentrations of bovine lactoperoxidase, human salivary peroxidase, and human myeloperoxidase.

Because of the important biological functions of peroxidases, there is growing interest in the measurement of their concentrations in various secretions. At present, there is no standard method which allows for comparisons in reported activities. This report describes procedures which can be used to measure peroxidase enzyme concentrations by commonly employed assays. Regression equations have been determined which can be used to calculate concentrations of bovine lactoperoxidase (LPO), human salivary peroxidase (SPO), and human myeloperoxidase (MPO) from activities measured with the following donors: pyrogallol, guaiacol, 2,2'-azinobis(3-ethylbenzylthiazoline-6-sulfonic acid), and thiocyanate (SCN-). The peroxidation rates of these donors depend upon the concentrations of hydrogen peroxide (H2O2) used in the individual assays and thus, for accurate, reproducible results, these concentrations must be carefully controlled. The SCN- normally present in human saliva will reduce observed reaction rates by simple competition kinetics in the ABTS, guaiacol and pyrogallol assays and will increase the rates observed when Cl- is used as a donor in NBS assay for MPO. Therefore, SCN- must be removed from saliva samples prior to peroxidase activity determination by all assays except the thionitrobenzoic acid (NBS) assay. LPO cannot be used as a standard for either SPO or MPO because the specific activities of LPO, SPO, and MPO are significantly different.

Animals↗

PubMed1986

Inhibition of mitochondrial respiration and production of toxic oxygen radicals by flavonoids. A structure-activity study.

A series of fourteen flavonoids were employed in a systematic structure-activity study to assess their abilities to inhibit succinoxidase and generate toxic oxygen species in beef heart mitochondria. By comparing I50 values toward succinoxidase activity, flavonoids with a catechol moiety on the b ring exhibited the following general order of potency: chalcone greater than flavone greater than flavonol greater than dihydroflavonol greater than anthocyanidin. Catechins were inactive. In a series of 3,5,7-trihydroxyflavones containing various configurations of the b ring hydroxyl groups, it was found that the flavonoids possessing adjacent trihydroxy (pyrogallol) and b ring ortho-hydroxy(catechol) configurations were the most potent inhibitors of succinoxidase, followed by those with meta-hydroxyl, monohydroxyl and unhydroxylated configurations. Four of the fifteen flavonoids tested exhibited substrate-independent, KCN-insensitive respiration. Two flavonols with a pyrogallol configuration, myricetin and quercetagetin, produced the largest respiratory bursts and were found to auto-oxidize. Evidence is presented that the mitochondrial respiratory bursts induced by both flavonols and their auto-oxidation resulted in the generation of O-2 and H2O2.

Animals↗