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PubMed2003

Discrimination of guests encapsulation in large hexameric molecular capsules in solution: pyrogallol[4]arene versus resorcin[4]arene capsules.

NMR experiments demonstrate that, although 2b and 3b form hexameric capsules in chloroform solutions and despite the very similar building units of these hexamers, 3b encapsulates only the noncharged trialkylamines while 2b can encapsulate both the noncharged trialkylamines and the respective ammonium salts obtained by the addition of DCl. In fact, it was found that protonation that forms in situ the ammonium salt ejects the guest from the hexameric capsule of 3b. This is a general observation as it was found for guests containing alkyl chains of four, five, six, and eight carbons.

Journal Article↗
PubMed2004

Tin(IV) chloride-chiral pyrogallol derivatives as new Lewis acid-assisted chiral Brønsted acids for enantioselective polyene cyclization.

[reaction: see text] New Lewis acid-assisted Brønsted acids (LBAs), tin(IV) chloride-2,6-dialkoxyphenols, serve as artificial cyclases for biomimetic polyene cyclization. For example, the enantioselective cyclization of 4-(homogeranyl)toluene using tin(IV) chloride-2,6-di[(1'R,2'R)-trans-2'-(3' ',5' '-xylyl)cyclohexanoxy]phenol gave a trans-fused tricyclic compound with 85% ee.

Journal Article↗
PubMed2005

Characterization and purification of polyphenol oxidase from artichoke (Cynara scolymus L.).

In this study, the polyphenol oxidase (PPO) of artichoke (Cynara scolymus L.) was first purified by a combination of (NH(4))(2)SO(4) precipitation, dialysis, and a Sepharose 4B-L-tyrosine-p-aminobenzoic acid affinity column. At the end of purification, 43-fold purification was achieved. The purified enzyme migrated as a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Polyacrylamide gel electrophoresis indicated that PPO had a 57 kDa molecular mass. Second, the contents of total phenolic and protein of artichoke head extracts were determined. The total phenolic content of artichoke head was determined spectrophotometrically according to the Folin-Ciocalteu procedure and was found to be 425 mg 100 g(-1) on a fresh weight basis. Protein content was determined according to Bradford method. Third, the effects of substrate specificity, pH, temperature, and heat inactivation were investigated on the activity of PPO purified from artichoke. The enzyme showed activity to 4-methylcatechol, pyrogallol, catechol, and L-dopa. No activity was detected toward L-tyrosine, resorsinol, and p-cresol. According to V(max)/K(m) values, 4-methylcatechol (1393 EU min(-1) mM(-1)) was the best substrate, followed by pyrogallol (1220 EU min(-1) mM(-1)), catechol (697 EU min(-1) mM(-1)), and L-dopa (102 EU min(-1) mM(-1)). The optimum pH values for PPO were 5.0, 8.0, and 7.0 using 4-methylcatechol, pyrogallol, and catechol as substrate, respectively. It was found that optimum temperatures were dependent on the substrates studied. The enzyme activity decreased due to heat denaturation of the enzyme with increasing temperature and inactivation time for 4-methylcatechol and pyrogallol substrates. However, all inactivation experiments for catechol showed that the activity of artichoke PPO increased with mild heating, reached a maximum, and then decreased with time. Finally, inhibition of artichoke PPO was investigated with inhibitors such as L-cysteine, EDTA, ascorbic acid, gallic acid, d,L-dithiothreitol, tropolone, glutathione, sodium azide, benzoic acid, salicylic acid, and 4-aminobenzoic acid using 4-methylcatechol, pyrogallol, and catechol as substrate. The presence of EDTA, 4-aminobenzoic acid, salicylic acid, gallic acid, and benzoic acid did not cause the inhibition of artichoke PPO. A competitive-type inhibition was obtained with sodium azide, L-cysteine, and d,L-dithiothreitol inhibitors using 4-methylcatechol as substrate; with L-cysteine, tropolone, d,L-dithiothreitol, ascorbic acid, and sodium azide inhibitors using pyrogallol as substrate; and with L-cysteine, tropolone, d,L-dithiotreitol, and ascorbic acid inhibitors using catechol as a substrate. A mixed-type inhibition was obtained with glutathione inhibitor using 4-methylcatechol as a substrate. A noncompetitive inhibition was obtained with tropolone and ascorbic acid inhibitors using 4-methylcatechol as substrate, with glutathione inhibitor using pyrogallol as substrate, and with glutathione and sodium azide inhibitors using catechol as substrate. From these results, it can be said that the most effective inhibitor for artichoke PPO is tropolone. Furthermore, it was found that the type of inhibition depended on the origin of the PPO studied and also on the substrate used.

Catechol Oxidase↗
PubMed1999

Effects of the superoxide dismutase-mimic compound TEMPOL on oxidant stress-mediated endothelial dysfunction.

The aim of this study was to investigate the effects of oxidant stress on endothelium-dependent and endothelium-independent arterial relaxation. For this, oxidant stress was generated by preincubation of rat aortic rings (RARs) in either 25 mM glucose (mimicking hyperglycemic stress) or 0.5 mM pyrogallol (a superoxide generator) and the effects of the superoxide dismutase (SOD)-mimetic compound 4-hydroxy-2,2,6,6-tetramethylpiperidinyloxy free radical (TEMPOL) on the vasorelaxant and cGMP-producing effects of acetylcholine (ACh) and glyceryl trinitrate (GTN) in control RARs and RARs exposed to oxidant stress were examined. Pyrogallol, and to a lesser extent high glucose concentration, enhanced the contractile response of RARs to phenylephrine and markedly inhibited the vasorelaxant response to ACh. Although they existed, the inhibitory effects of high glucose and pyrogallol on the vasorelaxant response to GTN were less profound, especially with pyrogallol. Moreover, both pyrogallol and high glucose concentration inhibited the basal and the ACh-induced vascular cyclic guanosine monophosphate (cGMP) production. Treatment with TEMPOL (1-5 mM) slightly increased the ACh and GTN-induced cGMP levels in control RARs but had a significant effect in high glucose and pyrogallol-pretreated RARs. Additionally, concomitant treatment of RARs with TEMPOL (5 mM) abolished the difference in the relaxation response between control RARs and RARs exposed to either pyrogallol or high glucose concentration. These results further support the theory that reactive oxygen species (ROS), especially superoxide, play a key role in mediation of endothelial dysfunction accompanying diabetes, probably through their effects on the ability of the endothelium to synthesize, release or respond to endogenous nitric oxide (NO) or NO donated by nitrovasodilators.

Acetylcholine↗
PubMedDate not supplied

Peroxynitrite, the product of nitric oxide and superoxide, causes myocardial injury in the isolated perfused rat heart.

BACKGROUND: Recent studies have determined that the product of NO and superoxide is peroxynitrite (ONOO-), an anion with deleterious tissue-oxidant effects. OBJECTIVE: To examine the effects of ONOO- on the isolated perfused rat heart. Sprague-Dawley rat hearts were perfused with a cell-free, Krebs-Henseleit solution on a Langendorf perfusion apparatus. The hearts were subjected to 30 min infusions of vehicle (control); 10 mumol/l S-nitroso-N-acetylpenicillamine (SNAP), an NO donor; 10 mumol/l pyrogallol, a superoxide generator); 10 mumol/l SNAP plus 10 mumol/l pyrogallol, a mixture that generates peroxynitrite; or 10 mumol/l SNAP plus 10 mumol/l pyrogallol plus 300 U/ml superoxide dismutase. RESULTS: SNAP or pyrogallol alone had no effect on cardiac function at the concentration used; however, infusion of the combination of SNAP and pyrogallol resulted in significant decreases in left ventricular developed pressure (to 83 +/- 4%, P < 0.01, versus vehicle) and dp/dtmax (to 76 +/- 6.2%, P < 0.01, versus vehicle), and also resulted in a significant increase in production of lactic dehydrogenase (to 118 +/- 4%, P < 0.01, versus vehicle). The administration of superoxide dismutase with SNAP and pyrogallol reversed these deleterious effects. CONCLUSION: These results suggest that the formation of peroxynitrite significantly enhances the toxicities of .NO and O2.- and causes marked cardiac injury.

Animals↗
PubMed2002

Deoxygenation of polyhydroxybenzenes: an alternative strategy for the benzene-free synthesis of aromatic chemicals.

New synthetic connections have been established between glucose and aromatic chemicals such as pyrogallol, hydroquinone, and resorcinol. The centerpiece of this approach is the removal of one oxygen atom from 1,2,3,4-tetrahydroxybenzene, hydroxyhydroquinone, and phloroglucinol methyl ether to form pyrogallol, hydroquinone, and resorcinol, respectively. Deoxygenations are accomplished by Rh-catalyzed hydrogenation of the starting polyhydroxybenzenes followed by acid-catalyzed dehydration of putative dihydro intermediates. Pyrogallol synthesis consists of converting glucose into myo-inositol, oxidation to myo-2-inosose, dehydration to 1,2,3,4-tetrahydroxybenzene, and deoxygenation to form pyrogallol. Synthesis of pyrogallol via myo-2-inosose requires 4 enzyme-catalyzed and 2 chemical steps. For comparison, synthesis of pyrogallol from glucose via gallic acid intermediacy and the shikimate pathway requires at least 20 enzyme-catalyzed steps. A new benzene-free synthesis of hydroquinone employs conversion of glucose into 2-deoxy-scyllo-inosose, dehydration of this inosose to hydroxyhydroquinone, and subsequent deoxygenation to form hydroquinone. Synthesis of hydroquinone via 2-deoxy-scyllo-inosose requires 2 enzyme-catalyzed and 2 chemical steps. By contrast, synthesis of hydroquinone using the shikimate pathway and intermediacy of quinic acid requires 18 enzyme-catalyzed steps and 1 chemical step. Methylation of triacetic acid lactone, cyclization, and regioselective deoxygenation of phloroglucinol methyl ether affords resorcinol. Given the ability to synthesize triacetic acid lactone from glucose, this constitutes the first benzene-free route for the synthesis of resorcinol.

Journal Article↗
PubMed2004

Some biochemical properties of polyphenol oxidase from celery.

Polyphenol oxidase (PPO, EC 1.14.18.1) was extracted from celery roots (Apium graveolens L.) with 0.1 M phosphate buffer, pH 7.0. The PPO was partially purified by (NH4)2SO4 and dialysis. Substrate specificity experiments were carried out with catechol, pyrogallol, L-DOPA, p-cresol, resorcinol, and tyrosine. The Km for pyrogallol, catechol, and L-DOPA were 4.5, 8.3, and 6.2mM, respectively, at 25 degrees C. Data for Vmax/Km values, which represent catalytic efficiency, show that pyrogallol has the highest value. The optimum pH and temperature were determined with catechol, pyrogallol, and L-DOPA. Optimum pH was 7.0 for catechol and L-DOPA, and 7.5 for pyrogallol. Optimum temperatures for maximum PPO activity were 25 degrees C for pyrogallol, 40 degrees C for catechol, and 45 degrees C for L-DOPA. Heat inactivation studies showed a decrease in enzymatic activity at temperatures above 60 degrees C. The order of inhibitor effectiveness was: L-cysteine > ascorbic acid > glycine > resorcinol > NaCl.

Apium↗
PubMed2001

Generation of superoxide anion impairs histamine-induced increases in macromolecular efflux.

The first goal of this study was to determine the effect of generation of superoxide anion using pyrogallol on histamine-induced increases in macromolecular efflux. We used intravital microscopy and fluorescein isothiocyanate-dextran (FITC-dextran; MW 70K) to examine macromolecular extravazation from postcapillary venules in the hamster cheek pouch in response to histamine before and following topical application of vehicle or pyrogallol. Extravazation of macromolecules was quantitated by counting venular leaky sites. Histamine elicited reproducible increases in venular leaky sites before and during infusion of vehicle. In contrast, topical application of pyrogallol (0.5 mM) abolished histamine-induced increases in formation of venular leaky sites. Our second goal was to examine whether pyrogallol-induced inhibition of venular leaky site formation could be reversed by superoxide dismutase. Application of superoxide dismutase (300 U/ml) to the cheek pouch in the presence of pyrogallol restored histamine-induced increases in venular leaky sites. Thus, the generation of superoxide anion alters histamine-induced increases in macromolecular efflux. These results support the concept that disease states that produce oxidative stress may impair agonist-induced increases in microvascular permeability via inactivation of nitric oxide.

Animals↗
PubMed2002

O2(-)-mediated impairment of coronary arterial relaxation is prevented by overnight treatment with 1 nM beta-estradiol.

We tested the hypothesis that the ability of coronary arteries to withstand functional damage from superoxide (O(2)(-)) is altered by exposure of the arteries to a physiological concentration of beta-estradiol. Female porcine coronary arterial rings were incubated in an O(2)-CO(2) incubator, under normoxic conditions, at 37 degrees C for 22-24 h. Arteries were then placed in baths containing a physiological salt solution at 37 degrees C with 95% O(2)-5% CO(2) for isometric force recordings. In rings from 14 female pigs, vasorelaxation to A-23187 and diethylamine-NONOate (DEA-NONOate) was determined with and without prior 15-min exposure to 400 microM pyrogallol. Sensitivity (-logM ED(50)) and maximum relaxation to A-23187, but not DEA-NONOate, were significantly impaired by exposure to pyrogallol (pyrogallol treated: 7.39 +/- 0.09, 82 +/- 5%; control: 7.76 +/- 0.11, 99 +/- 1%, means +/- SE; P < 0.01 and P < 0.05, respectively). This effect was attenuated by concurrent exposure to equimolar ascorbate. Arterial rings from 12 separate female pigs were incubated for 22-24 h with or without 1 nM beta-estradiol before pyrogallol exposure. beta-Estradiol significantly enhanced arterial sensitivity to A-23187 and prevented pyrogallol impairment without affecting DEA-NONOate responses. Therefore, superoxide-mediated endothelial damage and impaired endothelium-dependent relaxation of coronary arteries are prevented by overnight exposure of the arteries to a physiological concentration of beta-estradiol.

Animals↗