Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GALLIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,297 records · Page 72Linked to original sources
PubMedDate not supplied

Radical modulation activity of benzo[a]phenothiazine.

12H-Benzo[a]phenothiazine generated radical(s) under alkaline conditions, and enhanced the radical intensity of sodium ascorbate and sodium 5,6-benzylidene-L-ascorbate. Phenothiazine and chlorpromazine hydrochloride did not produce radicals, nor affect the radical intensity of ascorbates. 12H-Benzo[a]phenothiazine scavenged the superoxide anion and hydroxyl radical, more efficiently than phenothiazine and chlorpromazine hydrochloride. The radical modulation activity of 12H-benzo[a]phenothiazine might explain at least in part the ability of this compound to induce monocytic differentiation and apoptosis in human myelogenous leukemic cell lines.

Antioxidants↗
PubMed2006

Inhibitory effects of black tea theaflavin derivatives on 12-O-tetradecanoylphorbol-13-acetate-induced inflammation and arachidonic acid metabolism in mouse ears.

Tea has been shown to possess several health beneficial properties primarily due to its polyphenolic content. The major polyphenolic compounds in black tea leaves are theaflavins (TFs) formed by oxidative coupling of catechins in tea leaves during its processing. In this paper, we report the characterization of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear inflammatory model and the inhibitory effects of major black tea TFs derivatives on this inflammation. In addition, the effect on inflammatory biomarkers, such as proinflammatory cytokines and arachidonic acid metabolites, are reported as well. A single topical application of TPA to ears of CD-1 mice induced a time- and dose-dependent increase in edema as well as formation of proinflammatory cytokine proteins interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) in mouse ears. A single topical application of equimolar of black tea constituents (TF, theaflavin-3-gallate, theaflavin-3'-gallate, and theaflavin-3,3'-digallate) strongly inhibited TPA-induced edema of mouse ears. Application of TFs mixture to mouse ears 20 min prior to each TPA application once a day for 4 days inhibited TPA-induced persistent inflammation, as well as TPA-induced increase in IL-1beta and IL-6 protein levels. TFs also inhibited arachidonic acid (AA) metabolism via both cyclooxygenase (COX) and lipoxygenase pathways. This observation was substantiated by decreased amounts of AA metabolites prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) levels. Combined application of TF and sulindac, a nonsteroidal anti-inflammatory drug resulted a significant synergetic anti-inflammatory effect. Oral administration of TFs or the hot water extract of black tea leaves also significantly inhibited TPA-induced edema in mouse ears. In conclusion, proinflammatory cytokines, IL-1beta and IL-6, as well as the intermediated metabolites of AA, PGE2, and LTB4 are good biomarkers for inflammation. Black tea constituents, TF and its derivatives, had strongly anti-inflammatory activity in vivo which may be due to their ability to inhibit AA metabolism via lipoxygenase and COX pathways.

Animals↗
PubMed1984

Relationships between the chemical constitution of aggregation inhibitors and human blood platelet response profile.

Gradually altered synthetic entities were employed as molecular probes, and arachidonic acid, ADP, human alpha-thrombin and the Ca2+ ionophore A23187 as aggregation-inducing agents, in a comprehensive study on the response profile of human blood platelets with an emphasis on the effects of exogenous and increased intracellular Ca2+. Corroborating further previous conclusions, some representative carbamoylpiperidine derivatives, at concentrations effecting substantial inhibition of ADP-induced aggregation, failed to retain that effect when 5.0 mM Ca2+ was introduced into the otherwise identical test medium; reference compounds chlorpromazine and propranolol registered corresponding inhibitory patterns. At increased concentrations the compounds' inhibitory potency was regenerated even in the presence of 5 mM Ca2+. In fact, in sufficiently high concentrations, the compounds were even capable of inhibiting aggregation elicited by 15 microM of the ionophore A23187; so did chlorpromazine and propranolol. Another set of congeners revealed the striking sensitivity of ionophore A23187-induced human blood platelet aggregation to the surface active potencies of inhibitor molecules. The loss in inhibitory potency was directly related to the lesser hydrophobic character of the molecule.

Adenosine Diphosphate↗
PubMed1986

Interleukin-1 stimulates granule exocytosis from human neutrophils.

The interaction of human polymorphonuclear neutrophilic leukocytes (neutrophils) with interleukin-1 (IL-1) resulted in a time- and concentration-dependent, selective, release of azurophil (myeloperoxidase, lysozyme) and specific (lysozyme, vitamin B12-binding protein) granule constituents. Myeloperoxidase (MPO) and lysozyme secretion was markedly attenuated if neutrophils were not exposed to cytochalasin B (CB) prior to contact with IL-1. Degranulation was significantly enhanced in the presence of extracellular calcium. IL-1-elicited granule exocytosis was inhibited by the intracellular calcium antagonist, 8-(N,N-diethylamino)-octyl-(3,4,5-trimethoxy) benzoate hydrochloride (TMB-8), a calmodulin antagonist, trifluoperazine (TFP), and an anion channel blocker, 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene (DIDS). An evaluation of the role of arachidonic acid metabolites in IL-1-induced neutrophil activation revealed a suppressive effect on enzyme release exerted by the lipoxygenase inhibitors, piriprost potassium (6,9,deepoxy-6,9-(phenylimino)-delta 6,8 -prostaglandin I1, U-60,257B) and NDGA (nordihydroguaiaretic acid), and a cyclooxygenase/lipoxygenase inhibitor, ETYA (5,8,11,14-eicosatetraynoic acid). These data describe the characteristics of IL-1 as a human neutrophil secretagogue, and enhance our insight into the mechanism of inflammatory cell activation with this monokine.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2006

Synthesis of myo-inositol 1,2,3-tris- and 1,2,3,5-tetrakis(dihydrogen phosphate)s as a tool for the inhibition of iron-gall-ink corrosion.

Two myo-inositol phosphates, myo-inositol 1,2,3-tris(dihydrogen phosphate) and myo-inositol 1,2,3,5-tetrakis(dihydrogen phosphate), have been synthesised in several steps from myo-inositol (in Chem. Abstr.: d-myo-inositol) in the form of their sodium salts. They were shown to prevent iron-gall-ink decay in cellulose items at the same level as phytic acid dodecasodium salt.

Corrosion↗
PubMed2004

Cooperation in signal transduction of extracellular guanosine 5' triphosphate and nerve growth factor in neuronal differentiation of PC12 cells.

Guanosine 5' triphosphate (GTP), acting synergistically with the nerve growth factor (NGF), enhances the proportion of neurite-bearing cells in cultures of PC12 rat pheochromocytoma cells. We studied the transduction mechanisms activated by GTP in PC12 cells and found that addition of GTP (100 microM) increased intracellular calcium concentration ([Ca(2+)](i)) in cells that were between 60 and 70% confluent. Addition of GTP also enhanced activation of NGF-induced extracellular regulated kinases (ERKs) and induced Ca(2+) mobilization. This mobilization, due to the activation of voltage-sensitive and ryanodine-sensitive calcium channels, as well as pertussis toxin-sensitive purinoceptors, modulates Ca(2+)-activated K(+) channels not involved in activation of ERKs. The results presented here indicate that GTP-triggered [Ca(2+)](i) increase may be a key event in GTP signal transduction, which can modulate activity of ERKs. The physiological importance of the GTP effect lies in its capacity to interact with the NGF-activated pathway to enhance neurite outgrowth from PC12 cells.

Animals↗
PubMed1996

Volume regulation and the efflux of amino acids from cells in incubated slices of rat cerebral cortex. II. Dependence on Ca2+ ions.

The efflux of gamma-aminoisobutyric acid (GABA) and L-glutamate from pre-loaded cells in rat cerebral cortical slices has been studied during interventions designed to affect the availability of intracellular Ca2+ during hyposmotic swelling and membrane depolarization due to raised extracellular K+. Calmodulin-dependent acceleration of amino acid efflux in hyposmotic media, with cell swelling less than would be predicted on the basis of perfect osmometric behaviour (see Ref. [1]), was unaffected by Ca-ionophore in the presence of external Ca2+ or by the omission of external Ca2+, but was suppressed by pre-exposure of slices to thapsigargin (2 microM), which is reported to deplete cytosolic Ca2+, and by TMB-8 (0.5 mM), which blocks release of Ca2+ from internal stores. TMB-8 also led to significant cell swelling. The effects of TMB-8 were reversed by Ca-ionophore. Raised external K+ (54 mM) led to accelerated amino acid efflux which required calmodulin activation and was blocked by (i) omission of external Ca2+, (ii) the voltage-sensitive Ca2+ channel blocker nifedipine (1 microM), (iii) the anion transport inhibitor DIDS (25 microM for GABA, 100 microM for L-glutamate, see Ref. [1]), and (iv) the -SH group acetylator N-ethylmaleimide. TMB-8 was without effect in high K+ media. These results suggest that while enhanced amino acids efflux probably occurs through the same population of Ca/calmodulin-dependent, DIDS-sensitive pathways following hyposmotic shock or membrane depolarization, the source of Ca2+ ions required for the activation of these pathways may depend upon which of these acceleratory stimuli is applied.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

Estimates of the theoretical maximum daily intake of erythorbic acid, gallates, butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) in Italy: a stepwise approach.

The three recent EU directives which fixed maximum permitted levels (MPL) for food additives for all member states also include the general obligation to establish national systems for monitoring the intake of these substances in order to evaluate their use safety. In this work, we considered additives with primary antioxidant technological function for which an acceptable daily intake (ADI) was established by the Scientific Committee for Food (SCF): gallates, butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT) and erythorbic acid. The potential intake of these additives in Italy was estimated by means of a hierarchical approach using, step by step, more refined methods. The likelihood of the current ADI to be exceeded was very low for erythorbic acid, BHA and gallates. On the other hand, the theoretical maximum daily intake (TMDI) of BHT was above the current ADI. The three food categories found to be main potential sources of BHT were "pastry, cake and biscuits", "chewing gums" and "vegetables oils and margarine"; they overall contributed 74% of the TMDI. Actual use of BHT in these food categories is discussed, together with other aspects such as losses of this substance in the technological process and percentage of ingestion in the case of chewing gums.

Adolescent↗
PubMed2001

Role of calcium and calcium-activated proteases in CYP2E1-dependent toxicity in HEPG2 cells.

The objective of this work was to investigate whether CYP2E1- and oxidative stress-dependent toxicity in HepG2 cells is mediated by an increase of cytosolic Ca2+ and activation of Ca2+-modulated processes. HepG2 cells expressing CYP2E1 (E47 cells) or control cells not expressing CYP2E1 (C34 cells) were preloaded with arachidonic acid (AA, up to 10 microm) and, after washing, incubated with iron-nitrilotriacetic acid (up to 100 microm) for variable periods (up to 12 h). Toxicity was greater in E47 cells than in C34 cells at all times and combinations of iron/AA tested. Cytosolic calcium increased with incubation time in both cell lines, but the increase was higher in E47 cells than in C34 cells. The rise in calcium was an early event and preceded the developing toxicity. Toxicity in E47 cells and the increase in Ca2+ were inhibited by omission of Ca2+ from the extracellular medium, and toxicity was restored by reincorporation of Ca2+. An inhibitor of Ca2+ release from intracellular stores did not prevent the toxicity or the increase in Ca2+, reflecting a role for the influx of extracellular Ca2+ in the toxicity. Reactive oxygen production was similar in media with or without calcium, indicating that calcium was not modulating CYP2E1-dependent oxidative stress. Toxicity, lipid peroxidation, and the increase of Ca2+ in E47 cells exposed to iron-AA were inhibited by alpha-tocopherol. E47 cells (but not C34 cells) exposed to iron-AA showed increased calpain activity in situ (40-fold). The toxicity in E47 cells mirrored calpain activation and was inhibited by calpeptin, suggesting that calpain activation plays a causal role in toxicity. These results suggest that CYP2E1-dependent toxicity in this model depends on the activation of lipid peroxidation, followed by an increased influx of extracellular Ca2+ and activation of Ca2+-dependent proteases.

Arachidonic Acid↗