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PubMed2006

Pro-oxidative effects of tea and polyphenols, epigallocatechin-3-gallate and epigallocatechin, on G6PD-deficient erythrocytes in vitro.

Glucose-6-phosphate dehydrogenase (G6PD)-deficient subjects are vulnerable to chemical-induced hemolysis if exposed to oxidative agents. Recent studies reported that green tea and its constituents might act as pro-oxidants. Our objective was to investigate effects of tea and its polyphenolic components on the oxidative status of human G6PD-deficient erythrocytes. Erythrocytes of G6PD-deficient (n = 8) and normal (n = 8) subjects were incubated with water extracts of 3 types of tea samples (black tea, green tea and decaffeinated green tea extract) and 6 polyphenols. The resulting levels of reduced glutathione (GSH) and glutathione disulphide (GSSG), methemoglobin and plasma hemoglobin were quantified by HPLC and biochemical assays. The tea extracts significantly reduced GSH and increased GSSG levels in G6PD-deficient erythrocytes in a dose-dependent manner (0.5-10 mg/ml), but not in normal erythrocytes. Similar dose-dependent responses to (-)-epigallocatechin (EGC) and (-)-epigallocatechin-3-gallate (EGCG), but not to the other polyphenols, were observed. In G6PD-deficient cells, GSH was reduced by 43.3% (EGC at 0.05 mg/ml) and 33.3% (EGCG at 0.5 mg/ml), compared with pre-challenged levels. The concentration of methemoglobin was increased significantly when challenged with tea extracts, and EGC. Plasma hemoglobin levels were higher in G6PD-deficient samples after exposure to tea extracts, EGCG, EGC and gallic acid, compared with those in normal blood. Tea extracts and polyphenols significantly altered the oxidative status of G6PD-deficient erythrocytes in vitro as demonstrated by the decrease of GSH, and increased GSSG, methemoglobin and plasma hemoglobin. Our data caution against the excessive consumption of concentrated tea polyphenolic products by G6PD-deficient subjects.

Adult↗
PubMed2006

[Studies on chemical constituents in roots of Rumex dentatus].

OBJECTIVE: To investigate the active constituents from Rumex dentatus. METHOD: Compounds were isolated by silica gel, Sephadex LH -20 and ODS column chromatography and identified by chemical and spectroscopic methods. RESULT: Ten compounds were obtained and identified as helonioside A (1), gallic acid (2), isovanillic acid (3), p-hydroxycinnamic acid (4), succinic acid (5), n-butyl-beta-D-fructopyranoside (6), quercetin (7), hexadecanoic acid 2, 3-dihydroxy propyl ester (8), beta-sitosterol (9) and daucosterol (10). CONCLUSION: Compounds 1, 3-6 and 8 were isolated from the genus of Rumex for the first time.

Fructose↗
PubMed1991

[Total synthesis of an analogue of schizandrin].

A schizandrin analogue 9, 1, 2, 3, 10, 11, 12-hexamethoxy-6,7-dihydroxy-cis-6,7-dimethyl dibenzocyclooctadiene, is one of the metabolites of schizandrin with comparable anti-convulsion activity. In this paper, compound 9 was synthesized from gallic acid through the following sequence of reactions: methylation, Henry condensation, reduction with Fe-FeCl3-HCl, intermolecular reductive coupling and intramolecular nonphenolic oxidative coupling, totally in seven steps. The intermediate 1,4-diaryl-2,3-dimethyl-2,3-butanediol (7) which is a mixture of erythro and threo isomers was converted by DDQ in TFA into compound 9 and another new compound 10 via a different reaction path.

Animals↗
PubMed1991

Catalytic function of tyrosine residues in para-hydroxybenzoate hydroxylase as determined by the study of site-directed mutants.

The role of protein residues in activating the substrate in the reaction catalyzed by the flavoprotein p-hydroxybenzoate hydroxylase was studied. X-ray crystallography (Schreuder, H. A., Prick, P.A.J., Wieringa, R.K., Vriend, G., Wilson, K.S., Hol, W.G. J., and Drenth, J. (1989) J. Mol. Biol. 208, 679-696) indicates that Tyr-201 and Tyr-385 form a hydrogen bond network with the 4-OH of p-hydroxybenzoate. Therefore, site directed mutants were constructed, converting each of these tyrosines into phenylalanines. Spectral (visible and fluorescence) properties, reduction potentials, and binding constants are very similar to those of wild type, indicating that there are no major structural changes in the mutants. In the absence of substrate, the mutants and wild type exhibit similar pH-dependent changes in the FAD spectrum. However, the enzyme-substrate complex of Tyr-201----Phe lacks an ionization observed in both wild type and Tyr-385----Phe, which preferentially bind the phenolate form of substrates. Tyr-201----Phe shows no preference, indicating that Tyr-201 is required to ionize the substrate. The mutants have less than 6% the activity of the wild type enzyme. The effects on catalysis were studied by stopped flow techniques. Reduction of FAD by NADPH is slower by 10-fold in Tyr-201----Phe and 100-fold in Tyr-385----Phe. When the reduced Tyr-201----Phe-p-hydroxybenzoate complex reacts with oxygen, a long-lived flavin-C(4a)-hydroperoxide is observed, which slowly eliminates H2O2 with very little hydroxylation. Thus, the role of Tyr-201 is to activate the substrate by stabilizing the phenolate. Tyr-385----Phe reacts with oxygen to form 25% oxidized enzyme, and 75% flavin hydroperoxide, which successfully hydroxylates the substrate. This mutant also hydroxylates the product (3, 4-dihydroxybenzoate) to form gallic acid.

4-Hydroxybenzoate-3-Monooxygenase↗
PubMed1990

Calcium-dependent natural killer and calcium-independent natural cytotoxic activities in an IL-2-dependent killer cell line.

Using a cloned murine cell line, NKB61A2, that concomitantly exhibits both NK and natural cytotoxic (NC) activities, we investigated the biochemical mechanisms involved in natural cell mediated cytotoxicity against NK-sensitive YAC-1 tumor cells and against the NC-sensitive WEHI-164 tumor cells. Recent reports have suggested that target cell lysis by cytotoxic lymphocytes occurs by either a calcium dependent and/or a calcium-independent mechanism(s). To determine the role of calcium in NK and NC activities of the NKB61A2 cell line, we evaluated the effect of: 1) extracellular Ca2+ depletion by the divalent cation chelator, EGTA, 2) Ca2+ influx blockade by the Ca2+ channel blocker verapamil, and 3) blocking of intracellular Ca2+ mobilization by 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8). We found that EGTA, verapamil, and TMB-8 were all capable of inhibiting NK activity, but they had little effect on NC activity of the NKB61A2 cells. Using 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide which are inhibitors of protein kinase C and calmodulin respectively, we determined that protein kinase C and calmodulin do play a role in the NK activity of NKB61A2 cells. 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine and N-(6-aminohexyl)-5-chloro-1-naphthalanesulfonamide, similar to Verapamil and TMB-8, had no effect on NC activity. Thus, the data indicate that the NK activity of NKB61A2 cells is calcium dependent whereas NC activity is not. These results may explain the disparate reports seen in the literature of calcium-dependent and -independent lysis of tumor cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Two distinct pathways of platelet-activating factor-induced hydrolysis of phosphoinositides in primary cultures of rat Kupffer cells.

Stimulation of rat Kupffer cells in primary culture with platelet-activating factor (PAF) caused a rapid hydrolysis of phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate with a concomitant increase in the levels of myo-inositol 1,4,5-trisphosphate and myo-inositol 1,4-bisphosphate. This phospholipase C-mediated hydrolysis of polyphosphoinositides was independent of extracellular Ca2+ but was inhibited by the intracellular Ca2+ antagonist TMB-8. A second slower response to PAF was characterized by deacylation of PI leading to the accumulation of glycerophosphoinositol (GPI). PAF-induced GPI synthesis was not inhibited by TMB-8. These effects of PAF were accompanied by initial transient mobilization of Ca2+ from intracellular stores followed by a rather slow influx of Ca2+ from the extracellular medium. PAF-stimulated deacylation and phosphodiesteric hydrolysis of inositol lipids were differentially affected by cholera toxin and pertussis toxin. Pretreatment of the Kupffer cells with either of these toxins caused inhibition of phospholipase C activity. Pertussis toxin also inhibited PAF-stimulated deacylation. However, cholera toxin itself stimulated GPI release and addition of PAF to the cholera toxin-treated cells caused a further increase in GPI release. Phorbol ester inhibited PAF-induced phosphodiesteric hydrolysis of phosphoinositides, but not deacylation. PAF-induced metabolism of phosphoinositides was inhibited by the PAF antagonist, U66985. These results suggest that PAF-induced phosphodiesteric hydrolysis and deacylation of inositol phospholipids are regulated via distinct mechanisms involving activation of separate G-proteins in rat Kupffer cells. Also the regulation of phosphoinositide metabolism by Ca2+ mobilization from two separate Ca2+ pools is indicated by this study.

Animals↗
PubMed1989

Thrombin induces a calcium transient that mediates an activation of the Na+/H+ exchanger in human fibroblasts.

The calcium dependence of growth factor-induced cytoplasmic alkalinization was determined in serum-deprived human fibroblasts (WS-1 cells). Intracellular pH (pHi) and intracellular calcium (Ca2+i) were measured using the fluorescent dyes 2',7'-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein and fura2, respectively. Thrombin (10 nM) induced an alkalinization (0.18 +/- 0.01 pH units, n = 23) that was Na+-dependent and amiloride-sensitive, suggesting that the alkalinization was mediated by the Na+/H+ exchanger. Thrombin treatment caused a transient increase in Ca2+i (325 +/- 39 nM, n = 12) that preceded the observed increase in pHi. The increases in Ca2+i and pHi were dependent on the concentration of thrombin. The thrombin-induced increase in Ca2+i occurred in the absence of external calcium indicating that thrombin released calcium from internal stores. Inhibition of the thrombin-induced increase in Ca2+i with 8-diethylaminooctyl 3,4,5-trimethoxybenzoate hydrochloride or bis-(o-aminophenoxy)ethane-N,N,N',N'- tetraacetic acid also inhibited the thrombin-stimulated increase in pHi. The calcium ionophore ionomycin was used to increase Ca2+i independent of growth factor stimulation. When Ca2+i was elevated with ionomycin, a concomitant increase in pHi was observed. The increase in pHi due to ionomycin was dependent on Na+ and sensitive to amiloride. The removal of external Ca2+i inhibited the ionomycin-induced elevation of both Ca2+i and pHi. The ionomycin-induced increases in Ca2+i and pHi were not inhibited by 8-diethylaminooctyl 3,4,5-trimethoxy-benzoate hydrochloride. The results suggest that thrombin treatment can activate the Na+/H+ exchanger, and this activation is mediated by an increase in Ca2+i.

Amiloride↗
PubMed1987

Inositol 1,4,5-trisphosphate releases Ca2+ from vacuolar membrane vesicles of oat roots.

In plant cells, transient changes in cytoplasmic Ca2+ levels can modulate numerous developmental processes. Ca2+ is accumulated in the vacuole via a H+/Ca2+ antiport system that is energized by the tonoplast H+-pumping ATPase. Inositol 1,4,5-triphosphate (InsP3), but not inositol 1,4-bisphosphate, myo-inositol 1-phosphate, or fructose 2,6-bisphosphate, caused a transient reduction of Ca2+ levels in tonoplast vesicles. The decrease was dependent on InsP3 concentration (Km apparent = 0.6 microM). The InsP3-induced Ca2+ release was blocked by the Ca2+ antagonist, 8-(N,N-diethylamino)-octyl 3,4,5-trimethoxybenzoate-HCl. These results suggest that the vacuolar membrane is one target site for InsP3 action and that InsP3 may operate as a second messenger in the mobilization of intracellular Ca2+ in plant cells.

Calcium↗
PubMed1987

The role of Ca2+ in hormonal imprinting of the Tetrahymena.

It is known from model experiments on Tetrahymena that primary exposure to a hormone induces receptor formation or amplification, in other words a hormonal imprinting. Substances acting on the intracellular Ca2+ level of the Tetrahymena, such as TMB-8, EDTA, EGTA, NiCl2 and La(NO3)3, interfered with hormonal imprinting of the unicellular to different degrees, and some of them influenced hormone (insulin, TSH) binding also independently of imprinting. Interference with the intracellular Ca-metabolism generally influenced imprinting by insulin and TSH, which were mediated by different mechanisms, to dissimilar degrees, or in opposite directions. On combined application of the agents acting on Ca-metabolism, their effects were additive. It appears that intact Ca-mediation is an essential prerequisite for normal hormonal imprinting.

Calcium↗
PubMed1985

Calcium requirements for increased complement receptor expression during neutrophil activation.

It has recently been shown that human neutrophils rapidly increase surface expression of membrane receptors for C3b (CR1) and C3bi (CR3) in response to chemoattractants and other stimuli. In the present studies, we used monoclonal antibodies and flow cytometry to assess the role of Ca2+ in this process. Stimulation with ionophore A23187 in the presence of 1.2 mM Ca2+ increased CR1 330% and CR3 650% compared with unstimulated cells at 37 degrees C. Because this indicated that increasing the cytosolic free Ca2+ caused increased receptor expression, we examined the role of Ca2+ in the response to other stimuli as well. Adding 1.2 mM Ca2+ or 5 mM EDTA to the media in which the polymorphonuclear leukocytes were suspended had no effect on the CR1 response to f-MLP or LTB4, whereas Ca2+ slightly enhanced and EDTA markedly inhibited the CR3 response to these stimuli. The effects of Mg2+-EGTA and EDTA were identical. TMB-8 (200 microM), which inhibits the release of Ca2+ from intracellular stores, completely blocked the increased expression of both receptors induced by fMLP or LTB4. Increased expression of both receptors was also prevented by the calmodulin antagonists chlorpromazine (50 microM) and trifluoperazine (10 microM), but not by chlorpromazine sulfoxide. Phorbol myristate acetate (0.1 ng/ml) increased CR1 230% and CR3 265%. Again Ca2+ and EDTA did not alter the CR1 response, whereas Ca2+ increased CR3 to 287% and EDTA reduced CR3 to 187% of control. TMB-8 (250 microM) completely blocked both CR1 and CR3 responses to this stimulus as well. Thus, release of intracellular Ca2+ is necessary and sufficient for increased CR1 expression in response to diverse stimuli, but maximal increases in CR3 expression require an additional influx of extracellular Ca2+. These results indicate that the mechanisms by which the surface expression of the two different complement receptors increase are different in their requirements for extracellular Ca2+. In comparison with the work of others, we suggest that the processes of increased complement receptor expression and secretion of granular enzymes may also differ.

Calcimycin↗
PubMed1984

Lag period for superoxide anion generation and lysosomal enzyme release from human neutrophils: effects of calcium antagonists and anion channel blockers.

Responses by human neutrophils to stimulation include superoxide anion generation and lysosomal enzyme release. Both of these responses occur after distinct lag periods. The effects of calcium antagonists and anion channel blockers on these lag periods were examined to discern some activation steps mediating the effects of the chemotactic peptide f-Met-Leu-Phe and the calcium ionophore A23187. The intracellular calcium antagonist TMB-8 and the calmodulin inhibitor trifluoperazine both lengthened the lag periods for superoxide anion generation with either stimulus. This effect was dependent on the concentration of antagonist employed. Similar results were obtained for lysosomal enzyme release in response to A23187, as measured by a rapid centrifugation technique. None of the antagonists altered the lag periods for azurophil granule secretion, as monitored by the 9-aminoacridine technique. These results suggest a role for intracellular free calcium and calmodulin-dependent reactions in activation of the superoxide anion generation system in response to either stimulus, and activation of lysosomal enzyme release system in response to A23187.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMedDate not supplied

[Bile-forming function of the liver in the white rat].

White male rats were exposed to hypokinesia of 4 to 30 days in duration. The exposure led to a moderate hypersecretion of gall which was more distinct in autumn and winter. The synthesis and secretion of gallic acid increased. The excretion of cholesterol also grew. The ratio of tauro- and glycoacids shifted in favor of the latter. The cholate cholesterol coefficient increased. These changes in gall formation during hypokinesia are closely related to disorders in lipid and carbohydrate metabolism, as well as in adrenal function.

Adrenal Glands↗
PubMed1982

Selective inhibition of platelet lipoxygenase by esculetin.

The effects of coumarin and its derivatives on rat platelet lipoxygenase and cyclooxygenase activities were studied. Esculetin (6,7-dihydroxycoumarin) was found to inhibit the lipoxygenase more strongly than the cyclooxygenase; its concentration for 50% inhibition (IC50) was 0.65 microM for platelet lipoxygenase and 0.45 mM for platelet cyclooxygenase. Esculin (the 6-glucoside of esculetin) and umbelliferone (7-hydroxy-coumarin) also selectively inhibited the lipoxygenase, though less strongly (IC50 = 290 and 500 microM, respectively). 4-Hydroxycoumarin and coumarin had no inhibitory effect on either enzyme at concentrations up to 1 mM. The mechanism of the lipoxygenase inhibition by esculetin was non-competitive. Other antioxidants (hydroquinone, gallic acid and ascorbic acid) were less inhibitory to both enzymes and showed little selectivity.

4-Hydroxycoumarins↗
PubMed1983

Fatal acorn poisoning in a horse: pathologic findings and diagnostic considerations.

Acorn poisoning was diagnosed in an 11-year-old Quarter Horse with signs of severe colic, tachycardia, hyperpnea, abdominal borborygmus, rectal tenesmus, and hemorrhagic diarrhea. The diagnosis was based on history and predisposing factors, clinical signs, laboratory data, acorn husks in the feces, the urinary gallic acid equivalent concentration, and necropsy findings. The most striking pathologic changes were gastrointestinal and mesenteric edema, ulcerative enterocolitis, and nephrosis.

Animals↗
PubMedDate not supplied

Antioxidative effect of extracts from Erodium cicutarium L.

Extracts from Erodium cicutarium L. (EC) and some standard substances present in EC extracts were tested for their antioxidative properties during Fe(2+)-induced triglyceride oxidation. Hydrophobic fractions such as petroleum ether (PEE), benzene (BE) and chloroform I (ChE I) extracts as well as hydrophilic fractions i.e. water (WE) and ethyl acetate (EAE) showed an antioxidative effect. Among the tested substances vitamin C and some polyphenolic compounds: tannin, (+)-catechin and gallic acid exhibited antioxidative activity, stronger than the one of the mentioned extracts.

Antioxidants↗
PubMed1996

Effects of lipid A on calcium homeostasis in renal proximal tubules.

It is clear that lipopolysaccharides (LPS) are responsible for the multiorgan failure often associated with endotoxemia. However, little is known of the direct effects of LPS on kidney cells. We examined the effects of lipid A, the biologically active component of LPS, on rat proximal tubule Ca++ homeostasis. Lipid A produced a rapid, transient, concentration-dependent rise in intracellular Ca++ concentration, [Ca++]i, as monitored by fura-2. At 50 micrograms/ml [Ca++]i rose to 138 +/- 12 nM (n = 4) above basal [Ca++]i levels. The response to lipid A was not significantly inhibited by chelating extracellular Ca++ with EGTA (5 mM). However, the rise in [Ca++]i was significantly inhibited by 8-(N,N-dimethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride) and thapsigargin (17 +/- 7 nM and 13 +/- 9 nM rise, respectively; P < .05). These data indicate that the rise in [Ca++]i induced by lipid A is due to release of intracellular stores, and not extracellular influx. We also examined the role of inositol 1,4,5-trisphosphate in the lipid A response. Lipid A caused a time-dependent increase in inositol 1,4,5-trisphosphate that paralleled the rise in [Ca++]i, suggesting the release in [Ca++]i is through an inositol 1,4,5-trisphosphate-mediated release of intracellular stores. The ability of lipid A to alter Ca++ homeostasis suggests a potential for LPS to directly alter proximal tubule physiology and renal function in vivo.

Animals↗
PubMedDate not supplied

Effect of methionine depletion on growth and apoptosis in various tumor cell lines.

Sodium ascorbate, sodium 5,6-benzylidene-L-ascorbate (SBA), gallic acid and caffeic acid induced apoptotic cell death in human myelogenous leukemic cell lines, and stimulated oxidation of methionine into methionine sulfoxide in the culture medium. When various tumor cell lines were cultured in methionine-free medium, their growth was nearly terminated at G1 phase of the cell cycle, producing much smaller number of apoptotic cells. Addition of methionine sulfoxide to the methionine-free medium did not stimulate the apoptosis induction. These data suggest that induction of apoptosis by ascorbates, gallate or by caffeate cannot be simply explained by methionine oxidation.

Antioxidants↗