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At least 55 records · Page 3Linked to original sources
PubMed1992

Action profiles of nitric oxide, S-nitroso-L-cysteine, SNP, and NANC responses in opossum lower esophageal sphincter.

Circular muscle strips from opossum lower esophageal sphincter were suspended in organ baths for measurement of isometric tension. Nonadrenergic noncholinergic (NANC) inhibitory nerves were stimulated by means of transmural field stimulation. This induced frequency-dependent relaxations of the muscle strips. Methylene blue (3 x 10(-6) M; inhibits guanylate cyclase) and pyrogallol (10(-4) M; generates superoxide anions) had no influence on relaxations, whereas oxyhemoglobin [10(-5) M; binds nitric oxide (NO) and other nitroso compounds extracellularly] inhibited relaxations at all frequencies. NO concentration dependently relaxed the muscle strips. Pyrogallol (10(-4) M) and methylene blue (3 x 10(-6) M) inhibited and oxyhemoglobin (10(-5) M) nearly abolished relaxation induced by NO. S-nitroso-L-cysteine caused concentration-dependent relaxations of the muscle strips, which were inhibited by pyrogallol (10(-4) M), whereas methylene blue (3 x 10(-6) M) augmented the action of S-nitroso-L-cysteine. Methylene blue (3 x 10(-6) M) had no influence on the concentration-dependent relaxations caused by sodium nitroprusside (SNP). Oxyhemoglobin (10(-5) M), and to a lesser extent pyrogallol (10(-4) M), both inhibited the effects of SNP. The action profiles for S-nitroso-L-cysteine, NO, and SNP differed from the action profile for NANC nerve-mediated response. Although pyrogallol inhibited the effects of SNP, the action profile generally resembled the action profile for NANC responses more closely than did the profiles for S-nitroso-L-cysteine or NO. In conclusion, of the nitroso compounds studied, SNP most closely resembled the response to NANC nerve stimulation. Neither NO nor S-nitroso-L-cysteine individually mimicked the NANC response.

Animals↗
PubMed1992

Endothelium-dependent tolerance to ethanol-induced contraction of rat aorta: effect of inhibition of EDRF action and nitric oxide synthesis.

In vitro ethanol induces a dose-dependent contraction of the aorta. Tolerance to this effect of ethanol is expressed by a rightward shift of the dose-response curve in aorta from animals intoxicated with ethanol for 2 days. The expression of tolerance in the aorta is dependent upon the presence of functional endothelial cells which suggests that tolerance is mediated, in part, by endothelium-derived relaxing factor (EDRF). To test this hypothesis, three inhibitors of EDRF action and an inhibitor of nitric oxide synthesis were studied for their ability to alter tolerance to ethanol-induced contraction of the aorta. In vitro pretreatment of aortic rings with gossypol (10(-6)-10(-5) M), pyrogallol (10(-5) M), hemoglobin (10(-6) M), and NG-nitro-L-arginine (NOARG, 10(-4) M) inhibited endothelium-dependent relaxation induced by carbachol. The inhibition of carbachol-induced relaxation produced by pyrogallol was reversed by superoxide dismutase (SOD, 45 units/ml). In vitro pretreatment of rings obtained from ethanol-treated rats with gossypol, pyrogallol, hemoglobin, or NOARG inhibited the expression of ethanol tolerance, shifting the ethanol dose-response curve to control values. SOD reversed the effect of pyrogallol pretreatment. None of the antagonists significantly altered the ethanol dose-response curve of aortic rings obtained from control animals. These data support the hypothesis that tolerance to ethanol-induced contraction of the aorta is mediated by the release of EDRF from endothelial cells.

Animals↗
PubMedDate not supplied

[Possibilities for the deep bacterial destruction of 2,4,6-trinitrotoluene].

The possibility of 2,4,6-trinitrotoluene (TNT) deep destruction (the aromatic cycle fission inclusive) by Pseudomonas fluorescens B-3468 is reported for the first time. The formation of nitrogen-free metabolites, viz. phloroglucinol and pyrogallol, is preceded by the NAD(P)H-dependent deamination of 2,4-diamino-6-nitrotoluene (2,4-DA), a TNT intermediate. 30% of 2,4-DA nitrogen in released as ammonium under the action of an induced cell-free extract in the presence of the preferential co-factor NADH (together with FAD). The elevated pyrogallol-decomposing activity in cells grown on 2,4-DA, phloroglucinol and pyrogallol as well as the induction of the pyrocatechase activity in cells grown on the above substrates, together with the earlier reported accumulation of phloroglucinol and pyrogallol upon 2,4-DA utilization, indicated that the enzyme might be involved in the TNT cycle cleavage. The participation of NADH-dependent glutamate dehydrogenase in 2,4-DA nitrogen utilization is supported by experimental evidence.

Biodegradation, Environmental↗
PubMedDate not supplied

Vasodilatory activity of etozoline in rat and guinea-pig isolated aorta: study of the mechanism of action.

In isolated rings of guinea-pig aorta not responding to acetylcholine, the diuretic etozoline did not influence basal vascular tone but inhibited noradrenaline- and histamine-induced contractions. The inhibition was evident at concentrations of the diuretic (10 microM-1 mM) suitable to inhibit, in a competitive manner, the contractions evoked by a K+ channel blocker, tetraethylammonium, in the same preparation (Dorigo et al., 1989, 1990). In isolated rings of guinea-pig aorta, etozoline, at very low concentrations (1 nM-0.1 microM), inhibited also serotinin-induced contractions. The contractile effect of serotonin was abolished by nifedipine associated with 2-nitro-4-carboxyphenyl N,N-diphenyl-carbamate (an inhibitor of phospholipase C) or with etozoline, thus suggesting that the diuretic, besides inhibiting extracellular Ca++ uptake, also prevents intracellular Ca++ mobilization mediated by inositol triphosphate. In isolated rings of rat aorta responding to acetylcholine, etozoline did not influence basal vascular tone either in the absence or in the presence of superoxide-dismutase. In the same preparation, the diuretic inhibited vascular contractions induced by the three spasmogenic agents used, i.e. noradrenaline, histamine and serotonin. This inhibition occurred at concentrations of etozoline ranging from 10 microM to 1 mM and was uninfluenced by indomethacin (10 microMs). In isolated rings of rat aorta, the contractile effect of noradrenaline was not influenced by the addition of either 100 microM pyrogallol, or 10 microM methylene blue or 100 U/ml superoxide-dismutase, while the contractile responses to histamine and to serotonin were potentiated by pyrogallol and by methylene blue and reduced by superoxide-dismutase. This indicates that, in rat aorta, noradrenaline evokes only a direct contractile response, whereas both serotonin and histamine have a double effect: direct contraction of vascular smooth muscle and release of a relaxing factor from the endothelium. The inhibitory activity of etozoline towards serotonin- and histamine-induced contractions was reduced by pyrogallol and by methylene blue, whereas it was potentiated by superoxide-dismutase. The ability of etozoline to reverse the noradrenaline-induced contraction was unaffected by pyrogallol, methylene blue or superoxide-dismutase. These results emphasize the spasmolytic activity of etozoline, which seems to involve only the muscular component of rat and guinea-pig aorta.

Acetylcholine↗
PubMed1992

Vascular bound recombinant extracellular superoxide dismutase type C protects against the detrimental effects of superoxide radicals on endothelium-dependent arterial relaxation.

Extracellular superoxide dismutase type C (EC-SOD C) is a secretory SOD isoenzyme that, in vivo, is bound to heparan sulfate proteoglycans in the glycocalyx of various cell types (e.g., endothelial cells) and in the connective tissue matrix. The aim of this study was to investigate the efficacy of vascular bound EC-SOD C in protecting arterial relaxation mediated by endothelium-derived relaxing factor (EDRF) against the inhibitory effects of superoxide radicals. For comparison, the effect of CuZn SOD was also studied. This SOD isoenzyme lacks affinity toward heparan sulfate and does not bind to cell surfaces. Rings from rabbit aorta were mounted in an organ bath and acetylcholine-induced endothelium-dependent relaxation was then studied in preparations precontracted with phenylephrine. Pyrogallol (10(-4) M), used to generate superoxide radicals, reduced the maximal relaxant effect of acetylcholine from about 65% to 25%. When present in the buffer throughout the experiment, CuZn SOD and EC-SOD C caused a concentration-dependent prevention of the pyrogallol effect on EDRF-mediated relaxation, with a half-maximal effect at about 100 units/ml (KO2 assay). In a second set of experiments, the arterial rings were preincubated with 8,000 units/ml CuZn SOD (50 micrograms/ml) or EC-SOD C (69 micrograms/ml) during 30 minutes, followed by washing, before the effect of pyrogallol on EDRF-mediated relaxation was studied in SOD-free buffer.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1986

[Relation of the antimutagenic activity of simple phenols to the number of hydroxyl groups].

The influence of mono-phenol, di-resorcinol and tri-pyrogallol hydroxyl groups of simple unsubstituted phenols on the mutagenic potentials of benzo(a)pyrene was studied in vivo (micronuclear test on bone marrow polychromatic erythrocytes) and in vitro (test of direct point mutations at V79/HGPRT system induced by metabolic activation by mouse liver microsomal enzymes). The phenols decreased the mutagenic activity of benzo(a)pyrene in in vivo tests, with pyrogallol being the most active, it followed by resorcinol and phenol. The mixtures of benzo(a) pyrene + pyrogallol and benzo(a)pyrene + resorcinol were significantly less mutagenic in in vitro tests than benzo(a)pyrene and benzo(a)pyrene + phenol.

Animals↗
PubMed1991

Aluminum effect on the activity of superoxide dismutase and of other antioxygenic enzymes in vitro.

The effect of Al on superoxide dismutase (SOD) and on other antioxygenic enzymes: horseradish peroxidase, catalase, and glutathione peroxidase, has been investigated in vitro. In the case of SOD, the effect of metal chelators (EDTA and deferoxamine) and a possible synergistic effect with iron salts have also been tested using the pyrogallol assay. There is no significant inhibitory effect of Al on the activity of any of the above-mentioned enzymes. Noticeable increases in SOD activity were observed when metal chelators were added to the medium, but not when high concentrations of Al were present too, in the case of deferoxamine (DFO). The former fact seems to be a consequence of the chelation of transition metal ions that catalyze pyrogallol autoxidation by a mechanism not inhibitable by SOD, interfering in its action, which may account for part of the DFO antioxidant effect observed in vivo. The latter phenomenon could be owing to a saturation of the chelating capacity of DFO by an excess of Al present in the medium, which should bring the system back to the interfering conditions explained above. It can be concluded that Al, either in the presence or in the absence of iron salts, does not inhibit SOD activity in vitro. Moreover, no significant binding of Al to SOD was demonstrated, and the amounts of its metal constituents, Cu and Zn, were not affected by preincubation of the enzyme with Al. The effect of the different compounds tested on the rate of autoxidation of the indicating scavenger, pyrogallol, and a suitable hypothesis on their role in the oxidation process are also discussed.

Aluminum↗
PubMed1992

Determination of tannic acid and its phenolic metabolites in biological fluids by high-performance liquid chromatography.

A method for the identification and determination of tannic acid and its phenolic metabolites in biological fluids by high-performance liquid chromatography was developed. Tannic acid and four phenolic compounds, namely gallic acid, pyrogallol, 4-O-methylgallic acid and ellagic acid, were successfully extracted from the biological fluids by using ethyl acetate at acidic conditions. Gallic acid, pyrogallol and 4-O-methylgallic acid were found in the sheep urine, gallic acid, 4-O-methylgallic acid and ellagic acid in plasma, and gallic acid and ellagic acid in abomasal fluid after abomasal dosing of tannic acid. Tannic acid was found in the plasma apart from the abomasal fluid into which it was administered. The concentrations of tannic acid, gallic acid, pyrogallol, 4-O-methylgallic acid and ellagic acid in plasma, abomasal fluid and urine were measured. This method could be applied to measurement of other hydrolysable tannins and their phenolic metabolites in biological materials.

Abomasum↗
PubMed1990

Comparison of four indirect methods for fluid superoxide dismutase activities.

Relatively small sample dilutions could render fluid extracellular (EC) superoxide dismutase (SOD) activity assays more subject to interfering compounds than tissue SOD assays. Highly variable relative SOD activities were obtained when comparing four indirect assays for several fluid samples (human plasma, human synovial fluid, and plasma from healthy or inflamed rats). Analysis of rat plasma fractionated with Sephadex G-150 showed that each assay (three xanthine oxidase based assays plus a modified pyrogallol assay) detected apparent SOD activity almost entirely at the same molecular weight as rat lung EC SOD. However, unfractionated fluid samples caused interferences with the xanthine oxidase based SOD assays, though not with the pyrogallol method. Example of interference were stimulation of xanthine oxidase activity, color formation without xanthine oxidase, color formation despite excess Cu-Zn SOD addition, and absorbance changes with cyanide inhibition of EC SOD that were above or below blank values. In summary, relative fluid SOD values depended on the assay used, and a modified pyrogallol assay was not subject to several interferences found for three xanthine oxidase based assays of fluid SOD activity.

Animals↗
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↗
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↗