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At least 19 recordsLinked to original sources
PubMed2001

The kinetics and mechanisms of the reactions of aluminium(III) with gallic acid, gallic acid methyl ester and adrenaline.

The kinetics and mechanisms of the reactions of gallic acid, gallic acid methyl ester and adrenaline with aluminium(III) have been investigated in aqueous solution at 25 degrees C and an ionic strength of 0.5 M. A mechanism has been proposed which accounts satisfactorily for the kinetic data. This is consistent with a mechanism in which complex formation takes place almost exclusively by reaction of [Al(H2O)5OH]2+ with the ligands. [Al(H2O)5OH]2+ reacts with gallic acid, gallic acid methyl ester and adrenaline with rate constants of 1145, 1330 and 316 M(-1) s(-1) respectively. These data together with the equilibrium data enable the rate constants for reaction of [Al(H2O)6]3+ with both gallic acid and gallic acid methyl ester to be calculated. In view of the dissociative nature of water exchange on [Al(H2O)6]3+ and [Al(H2O)5(OH)]2+ the complex formation rate constants are discussed in terms of the Eigen-Wilkins-Tamm mechanism. The overall mechanisms have been validated using global analysis. The results are compared with previously published data on the complex formation reactions of aluminium(III). In addition, the rate constants and mechanisms for replacement of maltol by gallic acid methyl ester and diethylenetriaminepentaacetic acid (dtpa) have been investigated.

Aluminum↗
PubMed2001

The kinetics and mechanisms of the reaction of iron(III) with gallic acid, gallic acid methyl ester and catechin.

The kinetics and mechanisms of the reactions of a number of pyrogallol-based ligands with iron(III) have been investigated in aqueous solution at 25 degrees C and ionic strength 0.5 M NaClO(4). Mechanisms have been proposed which account satisfactorily for the kinetic data. These are generally consistent with a mechanism in which the 1:1 complex that is formed initially when the metal reacts with the ligand subsequently decays through an electron transfer reaction. There was also some evidence for the formation of a 1:2 ligand-to-metal complex at higher pH values. The kinetics of complex formation were investigated with either the ligand or metal in pseudo-first-order excess. Rate constants for k(1) of 2.83(+/-0.09)x10(3), 1.75(+/-0.045)x10(3) and 3300(+/-200) M(-1) s(-1) and k(-1) of 20(+/-6.0), 35(+/-13) and 25+/-7.6 M(-1) s(-1) have been evaluated for the reaction of Fe(OH)(2+) with gallic acid, gallic acid methyl ester and catechin, respectively. The stability constant of each [Fe(L)](+) complex has been calculated from the kinetic data. The iron(III) assisted decomposition of the initial iron(III) complex formed was investigated. Analysis of the kinetic data yielded both the equilibrium constants for protonation of the iron(III) complexes initially formed together with the rate constants for the intramolecular electron transfers for gallic acid and gallic acid methyl ester. All of the suggested mechanisms and calculated rate constants are supported by calculations carried out using global analysis of time-dependent spectra.

Catechin↗
PubMed1997

3,4,5-Trihydroxy benzoic acid (gallic acid), the hepatoprotective principle in the fruits of Terminalia belerica-bioassay guided activity.

Compound I isolated from fraction TB5 of Terminalia belerica and finally identified as 3,4,5-trihydroxy benzoic acid (gallic acid) was evaluated for its hepatoprotective activity against carbon tetrachloride (CCl4)-induced physiological and biochemical alterations in the liver. The main parameters studied were hexobarbitone-induced sleep, zoxazolamine induced paralysis, serum levels of transaminases and bilirubin. The hepatic markers assessed were lipid peroxidation, drug metabolising enzymes, glucose-6-phosphatase and triglycerides. Administration of Compound I led to significant reversal of majority of the altered parameters. Our results confirm the presence of hepatoprotective activity in altered parameters. Our results confirm the presence of hepatoprotective activity in Compound I.

Animals↗
PubMed1979

Relationship between the antibacterial activity towards Escherichia coli NCTC 5933 and the physico-chemical properties of some esters of 3,4,5-trihydroxybenzoic acid (Gallic acid).

Aqueous solubilities, oleyl alcohol: water and octanol: water partition coefficients, RM values, reduction in surface tension of water, relative antioxidant activities and pKa values, were determined for gallic acid and a series of its alkyl esters. Correlations were sought between these physico-chemical measurements and MIC, MBC and killing-rate determinations against Escherichia coli. Variations in antibacterial activity generally correlated well with partition parameters, but these correlations did not accurately predict the cut-off point in antibacterial activity.

Chemical Phenomena↗
PubMed2003

Gallic acid and gallic acid derivatives: effects on drug metabolizing enzymes.

Gallic acid and its structurally related compounds are found widely distributed in fruits and plants. Gallic acid, and its catechin derivatives are also present as one of the main phenolic components of both black and green tea. Esters of gallic acid have a diverse range of industrial uses, as antioxidants in food, in cosmetics and in the pharmaceutical industry. In addition, gallic acid is employed as a source material for inks, paints and colour developers. Studies utilising these compounds have found them to possess many potential therapeutic properties including anti-cancer and antimicrobial properties. In this review, studies of the effects of gallic acid, its esters, and gallic acid catechin derivatives on Phase I and Phase II enzymes are examined. Many published reports of the effects of the in vitro effects of gallic acid and its derivatives on drug metabolising enzymes concern effects directly on substrate (generally drug or mutagen) metabolism or indirectly through observed effects in Ames tests. In the case of the Ames test an antimutagenic effect may be observed through inhibition of CYP activation of indirectly acting mutagens and/or by scavenging of metabolically generated mutagenic electrophiles. There has been considerable interest in the in vivo effects of the gallate esters because of their incorporation into foodstuffs as antioxidants and in the catechin gallates with their potential role as chemoprotective agents. Principally an induction of Phase II enzymes has been observed however more recent studies using HepG2 cells and primary cultures of human hepatocytes provide evidence for the overall complexity of actions of individual components versus complex mixtures, such as those in food. Further systematic studies of mechanisms of induction and inhibition of drug metabolising enzymes by this group of compounds are warranted in the light of their distribution and consequent ingestion, current uses and suggested therapeutic potential. However, it must be noted that numerous constituents of foodstuffs have been found to be potent modulators of xenobiotic metabolism and the net human health effects may depend on concentrations of individual components and individual genetic makeup.

Animals↗
PubMed1995

Selective induction of cell death in cancer cells by gallic acid.

Gallic acid (3,4,5-trihydroxybenzoic acid) is a naturally occurring plant phenol obtained by the hydrolysis of tannins and is know to show some pharmacological activities. In screening anti-cancer agents in traditional Chinese medicines, gallic acid was found to show cytotoxicity against all cancer cells that we examined in this study (IC50s: 4.8-13.2 micrograms/ml). Gallic acid was found to show cytotoxicity against primary cultured rat hepatocytes and macrophages, and lesser cytotoxicity against fibroblasts and endothelial cells. Cell death in dRLh-84 cells occurred within 6h after gallic acid treatment at a concentration of more than 20 micrograms/ml. A study of structurally related compounds suggested that the cytotoxicity shown by gallic acid was not a common feature in phenolic compounds, but was a fairly specific characteristic of gallic acid. That is, three adjacent phenolic hydroxyl groups of gallic acid were responsible for the cytotoxicity, and the carboxyl group was not responsible, but seemed to be implicated in distinguishing between normal cells and cancer cells.

Animals↗
PubMed1992

Anti-inflammatory activity of gallic acid.

Gallic acid was found to possess antiinflammatory activity towards zymosan-induced acute food pad swelling in mice. In vitro studies on the mode of action of gallic acid revealed that this compound interferes with the functioning of polymorphonuclear leukocytes (PMNs). Scavenging of superoxide anions, inhibition of myeloperoxidase release and activity as well as a possible interference with the assembly of active NADPH-oxidase may account for the inhibition of inflammatory process by gallic acid. Structure-activity relationship analysis showed that the o-dihydroxy group of gallic acid is important for the inhibitory activity in vitro.

Animals↗
PubMed2000

Apoptosis-inducing activity of lipid derivatives of gallic acid.

Gallic acid derivatives with a lipophilic group (hydrogenated farnesyl gallate, lauryl gallate, gallic acid laurylamide and cholesteryl gallate) were examined for their ability to induce apoptosis in human monoblastic leukemia U937 cells. Farnesyl ester derivative is the most potent apoptosis inducer among the compounds examined. The results suggest that lipid derivatives can augment the apoptosis-inducing activity of gallic acid depending on the structure. These findings will provide useful information in developing anti-cancer agents.

Apoptosis↗
PubMed1998

Reactive oxygen species and intracellular Ca2+, common signals for apoptosis induced by gallic acid.

Gallic acid (3,4,5-trihydroxybenzoic acid), a naturally occurring plant phenol, induces cell death in apparently different manners, depending on cell lines. Flow cytometric analysis and agarose gel electrophoresis indicated that internucleosomal breakdown of chromatin DNA was observed in HL-60RG cells but not in dRLh-84, HeLa, and PLC/PRF/5 cells, and that the action of gallic acid was independent of cell cycle. A detailed study of signal transduction revealed that the gallic acid-induced cell death of all cells tested in this study was prevented by treatment with the intracellular thiol antioxidant N-acetyl-L-cysteine, catalase, and the intracellular calcium chelator bis-(o-aminophenoxy)-N,N,N,N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM). However, the effects of ascorbic acid, superoxide dismutase, EGTA, the endonuclease inhibitor zinc sulfate, the calmodulin inhibitor N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), and the NADPH oxidase inhibitor diphenyleneiodonium chloride on cell death were different depending on the cell type, suggesting that the death signal induced by gallic acid was diverse among different cell types, although the production of reactive oxygen species, such as H2O2, and the elevation of intracellular calcium concentration were required as common signals.

Animals↗
PubMedDate not supplied

Prooxidant action of two antioxidants: ascorbic acid and gallic acid.

The addition of two antioxidants, ascorbic acid or gallic acid to distilled water resulted in the rapid increase in the reduction potential, which a few seconds later was replaced with much higher oxidation potential. The addition of these compounds to culture medium dose-dependently increased the oxidation potential only. Ascorbic acid analogs, which had apoptosis-inducing activity, showed similar oxidation potential, whereas inactive analogs did not. The combination of ascorbate and hydrogen peroxide additively enhanced both the oxidation potential and cytotoxic activity. These data demonstrate that both ascorbic acid and gallic acid act as prooxidants for the induction of apoptotic cell death.

Antioxidants↗
PubMed1981

Reduction in antiviral activity of human beta interferon by gallic acid.

Gallic acid (GA) is a common part of the human diet, both in the free form and as a metabolite of tannic acid and propyl gallate. Cell cultures were incubated with mixtures of either GA and beta interferon (IFN-beta) (formerly fibroblast IFN) or medium and IFN-beta. The cells were subsequently challenged with virus. The virus plaque yields were greater in cells incubated with IFN-beta and GA than in cells incubated with IFN-beta and medium, indicating that in the former mixture, IFN-beta had lost antiviral activity. The magnitude of the loss was dependent upon the GA concentration. IFN-alpha and IFN-gamma (formerly leukocyte IFN and immune IFN, respectively) were not similarly affected. The effect of GA on IFN-beta could be reversed with 2-mercaptoethanol, suggesting a possible sulfhydryl involvement. Extensive dialysis of IFN-beta-GA mixtures to remove the GA failed to reverse the reduction in antiviral activity. This suggests that a direct and irreversible interaction between IFN-beta and GA took place, reducing the activity of IFN-beta. The significance of this finding with regard to virus infections of the intestine is discussed.

Binding Sites↗
PubMed2001

Catalase contents in cells determine sensitivity to the apoptosis inducer gallic acid.

Gallic acid (3,4,5-trihydroxybenzoic acid, GA) is known to induce apoptosis in cancer cells at lower IC50 values compared with values for normal cells. Apoptosis is inhibited completely by the addition of conditioned medium from cultured hepatocytes, whereas it is not prevented by conditioned media from tumor cells. We therefore studied the reason for the different response to GA-induced apoposis. GA-induced dRLh-84 cell death was completely abolished by the addition of peroxisome or cytosol as well as conditioned medium from primary cultured rat hepatocyte. As GA-induced cell death is known to be mediated by reactive oxygen species (ROS) and intracellular Ca2+, we determined the type of ROS generated by GA and found that GA generated hydrogen peroxide in culture medium. The addition of hydrogen peroxide generated by GA induced cell death in dRLh-84 cells. These results suggest that GA-induced cell death is mediated by hydrogen peroxide. On the other hand, the inhibitory activity of hepatocyte medium on GA-induced cell death was completely abolished by anti-catalase antibody. When the amount of catalase antigen was determined by Western blotting analysis, conditioned medium and the cytoplasm of hepatocytes contained high concentrations of catalase. Conditioned media from various tumor cell lines did not contain catalase, and the cytoplasm contained only low levels of catalase. These results show that GA-sensitive cells, including various tumor cells, produce only small amounts of catalase and secreted little enzyme into media, suggesting a lack of protective machinery against GA. In contrast, GA-insensitive cells, including hepatocytes, produce large amounts of catalase and release it in medium, resulting in the development of insensitivity to GA. In conclusion, catalase contents in cells determine different sensitivity to GA.

Animals↗
PubMed2003

Transepithelial transport of p-coumaric acid and gallic acid in Caco-2 cell monolayers.

The transepithelial transport of such common dietary phenolic acids as p-coumaric acid (CA) and gallic acid (GA) across Caco-2 cell monolayers was examined. CA transport was dependent on pH, and in a vectorial manner in the apical-basolateral direction. The permeation was concentration-dependent and saturable, the Michaelis constant and maximum velocity being 17.5 mM and 82.7 nmol min(-1) (mg of protein)(-1), respectively. Benzoic acid and acetic acid inhibited the permeation of CA. These results indicate that the transepithelial transport of CA was via the monocarboxylic acid transporter (MCT). On the other hand, the permeation of GA was not in a polarized manner, was independent of pH and linearly increased with increasing concentration of GA. The transport rate of GA was about 100 times lower than that of CA, suggesting the transepithelial transport of GA to be via the paracellular pathway. Dietary phenolic acids thus showed diversified characteristics in their intestinal absorption.

Adenocarcinoma↗
PubMed1975

Alternative routes of aromatic catabolism in Pseudomonas acidovorans and Pseudomonas putida: gallic acid as a substrate and inhibitor of dioxygenases.

When 3,4-dihydroxyphenylacetic acid (homoprotocatechuic acid) was added to Pseudomonase acidovorans growing at the expense of succinate, enzymes required for degrading homoprotocatechuate to pyruvate and succinate semialdehyde were strongly induced. These enzymes were effectively absent from cell extracts of the organism grown with 4-hydroxyphenylacetic acid, and this substrate was metabolized by the catabolic enzymes of the homogentisate pathway. Two separate ring-fission dioxygenases for 3,4,5-trihydroxybenzoic acid (gallic acid) were present in cell extracts of Pseudomonas putida when grown with syringic acid, and gallate was degraded by reactions associated with meta fission. One of the two gallate dioxygenases also attacked 3-O-methylgallic acid; the other, which did not, was induced when cells were exposed to gallate. This organism possessed ortho fission enzymes, including protocatechuate 3,4-dioxygenase (EC 1.13.11.3) and cis,cis-carboxymuconate-lactonizing enzyme (EC 5.5.1.2), after induction with 3,4-dihydroxybenzoic acid (protocatechuic acid). Gallate was a substrate for protocatechuate 3,4-dioxygenase, with a Vmax about 3% of that of protocatechuate and with an apparent Km slightly lower. Gallate was a powerful competitive inhibitor of protocatechuate oxidation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Mutants of phycomyces with decreased gallic acid content.

Most plants and some fungi accumulate phenols. Two hydroxybenzoic acids, gallic and protocatechuic acids, are abundant in the giant sporangiophores of the zygomycete Phycomyces blakesleeanus, much more so than in the basal mycelium or the culture medium. The actual concentrations vary with illumination, age of the culture, and composition of the medium. We devised a simple screening procedure to isolate hba mutants whose sporangiophores contained less gallic acid than the wild type. The most useful mutant had very low concentrations of hydroxybenzoic acids in the sporangiophores, but about the same as the wild type in the basal mycelium and the medium. The mutant was only slightly different from the wild type in growth and morphology. Mutant and wild-type sporangiophores grew away from ultraviolet C sources (260 nm) equally well. Contrary to previous conjectures, ultraviolet tropism does not depend on the ultraviolet absorption of gallic acid or other free hydroxybenzoic acids in the sporangiophore. Against expectations, phenols did not impair DNA extraction: sporangiophores produced better DNA preparations than basal mycelia and the hba mutant only slightly better than the wild type.

DNA, Fungal↗
PubMed1992

Antitumor-promoting activities of tannic acid, ellagic acid, and several gallic acid derivatives in mouse skin.

Naturally occurring plant phenols with antimutagenic and anticarcinogenic activities were tested for their abilities to inhibit the biochemical and biological effects of the potent tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) in mouse epidermis in vivo. When applied topically to mouse skin, tannic acid (TA), ellagic acid, and several gallic acid derivatives all inhibit TPA-induced ornithine decarboxylase activity, hydroperoxide production, and DNA synthesis, three biochemical markers of skin tumor promotion. Moreover, in the two-step initiation-promotion protocol, the same phenolic compounds also inhibit the incidence and yield of skin tumors promoted by TPA. TA is the most effective of these treatments. Since they are already known to inhibit tumor initiation, the plant phenols protecting against skin tumor promotion by TPA may be universal inhibitors of multistage carcinogenesis. TA and other polyphenols, therefore, might be valuable in cancer therapy and/or prevention.

Animals↗