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PubMed2001

Anti-tumor effect of gallic acid on LL-2 lung cancer cells transplanted in mice.

We previously reported that gallic acid (3,4,5-trihydroxybenzoic acid), a naturally occurring plant phenol, can induce apoptosis in four kinds of human lung cancer cell lines in vitro. The present study further investigated the in vivo anti-tumor effects of orally administered gallic acid. Gallic acid reduced cell viability of LL-2 mouse lung cancer cells in vitro dose dependently, with a 50% inhibitory concentration (IC50) value of around 200 microM. C57Black mice were transplanted with LL-2 cells, and administered gallic acid (1 mg/ml in drinking water, ad libitum) and/or cisplatin (4 mg/kg i.p. injection, once a week). The average weight of the transplanted tumors, obtained at 29 days after transplantation, in the mice of control, gallic acid-treated cisplatin-treated and cisplatin plus gallic acid-treated groups was 4.02, 3.65, 3.19 and 1.72 g, respectively. The average tumor weight of the mice treated with cisplatin combined with gallic acid was significantly smaller than that of the control group (p<0.05). The amount of apoptotic cells in the tumor tissues of mice treated with gallic acid and/or cisplatin was significantly higher than those of the control mice. Combination of gallic acid and cisplatin increased the tumor cell apoptosis compared with the treatment with cisplatin alone. The present findings suggest that the combination of gallic acid with an anti-cancer drug, including cisplatin, may be an effective protocol for lung cancer therapy.

Animals↗
PubMed1999

Cell death-inducing activity by gallic acid derivatives.

In this study, the cytotoxic activity of gallic acid derivatives (GDs) was studied using some cancer cell lines. Among them, 3,4-methylenedioxyphenyl 3,4,5-trihydroxybenzoate (GD-1) and S-(3,4-methylenedioxyphenyl)-3,4,5-trihydroxy-thiobenzoate (GD-3) were found to induce cell death in cancer cell lines with IC50s ranging from 2.9 to 114.4 microM, a concentration comparable with or lower than that of gallic acid. On the other hand, although gallic acid did not show any cytotoxicity against primary cultured rat hepatocytes and human keratinocytes, GD-1 and -3 showed slightly higher sensitivity against such normal cells, when compared with gallic acid. The cell death induced by gallic acid and GD-1 was accompanied by internucleosomal DNA fragmentation characteristic of apoptosis, whereas only smear DNA degradation was detected following GD-3 treatment. When the mechanism by which GD-1 and -3 caused cell death in HL-60RG cells was examined, GD-1 and -3-induced cell death was inhibited by the intracellular Ca2+ chelator, bis-(o-aminophenoxy)-N,N,N,N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM), calmodulin inhibitor, W-7, and the Ca2+/Mg2+ -dependent endonuclease inhibitor zinc sulfate. In contrast, catalase, N-acetylcysteine (NAC), and ascorbic acid inhibited gallic acid-induced apoptosis in HL-60RG cells, whereas they had no effect on GD-1- and -3-induced cell death. This result suggests that GD-1 and -3 induced cell death in a different manner to gallic acid. In conclusion, esterification of gallic acid with a 3,4-methylenedioxyphenyl group yielded potent agents to treat cancer with a different signaling pathway from gallic acid, although selectivity was lost.

Antineoplastic Agents, Phytogenic↗
PubMed2005

Interactions of tannic acid and its derivatives (ellagic and gallic acid) with calf thymus DNA and bovine serum albumin using spectroscopic method.

In the present investigation, an attempt has been made to study the interaction of chosen polyphenols (tannic, ellagic and gallic acids) with calf thymus DNA and bovine serum albumin (BSA) employing spectrofluorimetric technique. The fluorescence quenching of DNA-bound ethidium bromide (EB) and BSA-bound 1-anilinonaphthalene-8-sulfonic acid (ANS) by phenolic acids has been examined. As BSA contains two tryptophan residues, the polyphenols influence on protein by measuring the changes in the fluorescence of BSA in the presence of phenolic acids was also evaluated. Our experiments prove that there is a direct interaction between phenols and DNA or BSA. The obtained data suggest that used acids can intercalate to DNA and interact strongly with BSA. The strongest interactions were observed between DNA and ellagic acid and between BSA and tannic acid. The conformational changes were revealed in DNA and BSA after incubation with tested phenolic acids and the extent depended on the phenol structure and the used concentration.

Anilino Naphthalenesulfonates↗
PubMed2005

A rapid densitometric method for simultaneous quantification of gallic acid and ellagic acid in herbal raw materials using HPTLC.

Gallic acid and ellagic acid are two widely occurring phenolic compounds of plant origin, to which many biological activities including anticancer and antiviral activity have been attributed. A simple HPTLC method has been developed for the simultaneous quantification of gallic acid and ellagic acid. The method was validated for precision, repeatability, and accuracy. Instrumental precision was found to be 0.083 and 0.78, and the repeatability of the method was found to be 1.07 and 1.50 (% CV) for gallic acid and ellagic acid, respectively. The accuracy of the method was checked by a recovery study conducted at two different levels and the average percentage recovery was found to be 101.02% for gallic acid and 102.42% for ellagic acid. The above method was used for the quantification of gallic acid and ellagic acid content in seeds of Abrus precatorius Linn., whole plant of Phyllanthus maderaspatensis Linn., and flowers of Nymphaea alba Linn. The proposed HPTLC method for the simultaneous quantification of gallic acid and ellagic acid was found to be simple, precise, specific, sensitive, and accurate and can be used for routine quality control of herbal raw materials and for the quantification of these compounds in plant materials.

Abrus↗
PubMed1998

Purification and characterization of gallic acid decarboxylase from pantoea agglomerans T71

Oxygen-sensitive gallic acid decarboxylase from Pantoea (formerly Enterobacter) agglomerans T71 was purified from a cell extract after stabilization by reducing agents. This enzyme has a molecular mass of approximately 320 kDa and consists of six identical subunits. It is highly specific for gallic acid. Gallic acid decarboxylase is unique among similar decarboxylases in that it requires iron as a cofactor, as shown by plasma emission spectroscopy (which revealed an iron content of 0.8 mol per mol of enzyme subunit), spectrophotometric analysis (absorption shoulders at 398 and 472 nm), and inhibition of the enzyme activity by 2,2'-bipyridyl, o-phenanthroline, and EDTA. Another interesting feature of this strain is the fact that it contains a tannase, which is used together with the gallic acid decarboxylase in a two-enzyme resting cell bioconversion to synthesize valuable pyrogallol from readily available tannic acid.

Journal Article↗
PubMed1997

Retrobiosynthetic NMR studies with 13C-labeled glucose. Formation of gallic acid in plants and fungi.

The biosynthesis of gallic acid was studied in cultures of the fungus Phycomyces blakesleeanus and in leaves of the tree Rhus typhina. Fungal cultures were grown with [1-13C]glucose or with a mixture of unlabeled glucose and [U-13C6]glucose. Young leaves of R. typhina were kept in an incubation chamber and were supplied with a solution containing a mixture of unlabeled glucose and [U-13C6]glucose via the leaf stem. Isotope distributions in isolated gallic acid and aromatic amino acids were analyzed by one-dimensional 1H and 13C NMR spectroscopy. A quantitative analysis of the complex isotopomer composition of metabolites was obtained by deconvolution of the 13C13C coupling multiplets using numerical simulation methods. This approach required the accurate analysis of heavy isotope chemical shift effects in a variety of different isotopomers and the analysis of long range 13C13C coupling constants. The resulting isotopomer patterns were interpreted using a retrobiosynthetic approach based on a comparison between the isotopomer patterns of gallic acid and tyrosine. The data show that both in the fungus and in the plant all carbon atoms of gallic acid are biosynthetically equivalent to carbon atoms of shikimate. Notably, the carboxylic group of gallic acid is derived from the carboxylic group of an early intermediate of the shikimate pathway and not from the side chain of phenylalanine or tyrosine. It follows that the committed precursor of gallic acid is an intermediate of the shikimate pathway prior to prephenate or arogenate, most probably 5-dehydroshikimate. A formation of gallic acid via phenylalanine, the lignin precursor, caffeic acid, or 3,4, 5-trihydroxycinnamic acid can be ruled out as major pathways in the fungus and in young leaves of R. typhina. The incorporation of uniformly 13C-labeled glucose followed by quantitative NMR analysis of isotopomer patterns is suggested as a general method for biosynthetic studies. As shown by the plant experiment, this approach is also applicable to systems with low incorporation rates.

Carbon Isotopes↗
PubMed2003

Endothelium-dependent contraction of rat thoracic aorta induced by gallic acid.

The vascular effect of a component of hydrolysable tannins, gallic acid, was examined in isolated rat thoracic aorta. Gallic acid exerted a contractile effect on the phenylephrine- or prostaglandin F(2/alpha)-precontracted endothelium-intact arteries. In endothelium-denuded arteries, the contractile response to-gallic acid was absent. Pretreatment with N(G)-nitro-L-arginine methyl ester (30 microM) abolished the gallic acid-induced contraction. Pretreatment with indomethacin (10 microM) or BQ610 (100 nM) had no observed effect. Pretreatment with gallic acid (1-10 microM) significantly attenuated the relaxation induced by acetylcholine, and that with 10 microM gallic acid also reduced the potency of sodium nitroprusside in the relaxation, without a reduction in efficacy, in endothelium-denuded arteries. These findings indicate that gallic acid induced endothelium-dependent contraction and strongly inhibited the endothelium-dependent relaxation rather than the endothelium-independent relaxation, probably through inhibition of endothelial nitric oxide (NO) production. Since NO plays an important role in vasodilative regulation and inflammatory disorders, these findings may also indicate that gallic acid interferes with the inflammatory responses.

Acetylcholine↗
PubMed2000

Synthesis of gallic acid: Cu(2+)-mediated oxidation of 3-dehydroshikimic acid.

With the elaboration of high-yielding, high-titer syntheses of 3-dehydroshikimic acid from glucose using recombinant Escherichia coli, oxidation of this hydroaromatic becomes a potential route for synthesis of gallic acid. Conversion of 3-dehydroshikimic acid into gallic acid likely proceeds via initial enolization of an alpha-hydroxycarbonyl and oxidation of the resulting enediol. 3-Dehydroshikimate enolization in water was catalyzed by inorganic phosphate while Zn(2+) was used to catalyze enolization in acetic acid. Enediol oxidation employed Cu(2+) as either the stoichiometric oxidant or as a catalyst in the presence of a cooxidant. Gallic acid was produced in a yield of 36% when 3-dehydroshikimic acid in phosphate-buffered water reacted for 35 h with H2O2 and catalytic amounts of CuSO(4). 3-Dehydroshikimate-containing, phosphate-buffered culture supernatants reacted with stoichiometric amounts of CuCO(3)Cu(OH)(2) and Cu(x)(H(3-x)(PO4)(2) to give gallic acid in yields of 51% in 5 h and 43% in 12 h, respectively. Solutions of 3-dehydroshikimic acid in acetic acid reacted with stoichiometric amounts of Cu(OAc)(2) to afford a 74% yield of gallic acid in 36 h. Acetic acid solutions of 3-dehydroshikimic acid could also be oxidized by air using catalytic quantities of Cu(OAc)(2). ZnO accelerated these oxidations leading to a 67% yield of gallic acid in 4 h when an acetic acid solution of 3-dehydroshikimic acid was reacted with O(2) and a catalytic amount of Cu(OAc)(2).

Catalysis↗
PubMed2004

Inhibition of fucosyltransferase VII by gallic acid and its derivatives.

Gallic acid (GA) and several gallate derivatives were identified as inhibitors of fucosyltransferase VII (FucT VII). The inhibition by GA and (-)-epigallocatechin gallate (EGCG) is time-dependent and irreversible. GA and EGCG showed inhibition with IC(50) of 60 and 700 nM, respectively, after pre-incubation with FucT VII in the presence of MnCl(2). Absence of MnCl(2) results in significantly weaker inhibition. Complexation of Mn(2+) with GA, EGCG, and gallate esters was observed. Such complexation, however, is not rate-limiting for the inhibition of FucT VII. Therefore, time-dependent inhibition of fucosyltransferases by GA and EGCG is likely due to the slow inactivation by the inhibitors or Mn-inhibitor complex. Although Mg(2+) or Ca(2+) can replace Mn(2+) for FucT VII activation, none forms a complex with GA or EGCG and hence results in weaker inhibition of FucT VII. GA and EGCG also inhibit FucT IV and alpha2,3-(N)-sialyltransferase in the low micromolar range. The structure-function divergence could be observed, as EGCG, but not GA or gallate esters, inhibits Zn(2+) containing metalloproteases such as TNFalpha convertase, matrix metalloproteases 2 and 7.

Catechin↗
PubMed2006

Synthesis of gallic acid based naphthophenone fatty acid amides as cathepsin D inhibitors.

Gallic acid, one of the most abundant plant phenolic acids, has been modified to cathepsin D protease inhibitors. The strategy of modification was proposed basing on some previously reported structure and activity relationship (SAR) studies. The synthesized naphthophenone fatty acid amide derivatives have been evaluated for in vitro cathepsin D inhibition activity. Two of them have shown significant inhibition activity with IC(50) values of 0.06 and 0.14 microM, respectively, as compared against pepstatin (0.0023 microM), the most potent inhibitor known so far. The study revealed that such attempts on gallic acid based pharmacophores might result in potent inhibitors of cathepsin D.

Amides↗
PubMed2006

Rise in the pH of an unfrozen solution in ice due to the presence of NaCl and promotion of decomposition of gallic acids owing to a change in the pH.

Oxidative decomposition of gallic acid occurs in alkaline solutions but hardly arises in acidic solutions. We have found that the addition of sodium chloride promotes the decomposition of gallic acid caused by freezing even under neutral and acidic conditions. Even at pH 4.5, gallic acid was decomposed by freezing in the presence of NaCl; however, in the absence of NaCl, it was hardly decomposed by freezing at pH lower than 7. Chloride ions are more easily incorporated in ice than sodium ions when the NaCl solution is frozen. The unfrozen solution in ice becomes positively charged, and as a result, protons transfer from the unfrozen solution to the ice. We measured the pH in the unfrozen solution which coexists with single-crystal ice formed from a 5 mmol dm(-3) NaCl solution and determined the pH to be 8.6 at equilibrium with CO(2) of 380 ppm or 11.3 in the absence of CO(2) compared to pH 5.6 in the original solution. From the model calculation performed for gallic acid solution in the presence of 5 mmol dm(-3) NaCl, it can be estimated that the amount of OH(-) transferred from the ice to the solution corresponds to 1.26 x 10(-5) mol dm(-3). The amount of OH(-) transferred is concentrated into the unfrozen solution and affects the pH of the unfrozen solution. Therefore, the pH in an unfrozen gallic acid solution in ice becomes alkaline, and the decomposition of gallic acid proceeds. It is expected that other base-catalyzed reactions in weakly acidic solutions also proceed by freezing in the presence of NaCl without the need for any alkaline reagents.

Journal Article↗
PubMedDate not supplied

Cytotoxic activity of gallic acid against liver metastasis of mastocytoma cells P-815.

Gallic acid (3,4,5-trihydroxy benzoic acid), a naturally occurring plant phenol, inhibited the proliferation of metastatic tumor cells, such as P815 murine mastocytoma, B16 murine melanoma and L5178 murine lymphoma cells at IC50s of 6.5, 8.0 and 3.6 microg/ml, respectively. P815 mastocytoma cells are known to metastasize specifically to the liver. When DBA/2 mice, injected intravenously with P815 cells, were treated with gallic acid at a concentration of 50 mg/kg, the number of nodules in the liver and serum glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT), which had increased as liver metastasis progressed, decreased. However, gallic acid itself did not show a liver protective effect though the life span of DBA/2 mice was extended by gallic acid treatment. These results suggest that gallic acid is able to inhibit liver metastasis, by killing P815 cells metastasized to the liver.

Animals↗
PubMed1987

Degradation of gallic acid by Aspergillus flavus.

Aspergillus flavus utilized gallic acid as sole carbon source and increased in presence of glucose and sucrose. The enzymes were inducible in nature and during degradation of gallic acid. 4-carboxy, 2-hydroxy cis, cis-muconic acid and pyruvic acid were detected. The estradiol (meta) fission of gallic acid by A. flavus was postulated.

Aspergillus flavus↗
PubMedDate not supplied

Induction of apoptosis by gallic acid in human stomach cancer KATO III and colon adenocarcinoma COLO 205 cell lines.

Antitumor effects of gallic acid on human stomach cancer KATO III cells and human colon adenocarcinoma COLO 205 cells were investigated. The exposures of KATO III and COLO 205 cells to gallic acid led to both growth inhibition and induction of apoptosis. Morphological changes showing apoptotic bodies were observed in both the cell lines treated with gallic acid. The fragmentations by gallic acid of DNA to oligonucleosomal-sized fragments, that are characteristics of apoptosis, were observed to be concentration- and time-dependent. These findings suggest that growth inhibitions by gallic acid of KATO III cells and COLO 205 cells result from the apoptosis induced by gallic acid. Thus, gallic acid might be a candidate drug for digestive gut cancer treatment to overcome the resistance to chemotherapeutic drugs.

Adenocarcinoma↗
PubMed2002

Anti- and prooxidative properties of gallic acid in fenton-type systems.

The anti- and prooxidative properties of gallic acid in Fenton-type systems containing H(2)O(2) and Fe(III) were examined in pH 3-10 reaction media and at reaction temperatures of 20-50 degrees C. Although it is a free radical scavenger, gallic acid may exhibit prooxidative properties, as it promotes the production of hydroxyl radicals due to iron chelation. The overall effect is prooxidative if the ratio of the concentrations of gallic acid and Fe(III) in the reaction medium is smaller than 2. If the ratio is greater than 2, the overall effect of gallic acid presence is antioxidative due to free radical scavenging properties. The dependence of rates and of apparent activation energies of gallic acid consumption on pH in Fenton-type systems was also examined, and it is concluded that the rate-determining steps in acidic and alkaline media are different, the overall rate of gallic acid consumption being lowest at pH 7.

Antioxidants↗
PubMed1999

Induction of apoptosis by gallic acid in lung cancer cells.

The apoptosis-inducing effect of gallic acid (3,4,5-trihydroxybenzoic acid) was investigated in four human lung cancer cell lines, SBC-3 (small cell carcinoma), EBC-1 (squamous cell carcinoma), A549 (adenocarcinoma) and SBC-3/CDDP (cisplatin-resistant subclone of SBC-3). Gallic acid induced apoptosis in a dose-dependent manner as evidenced by analyses of DNA fragmentation, changes in cell morphology and loss of viability. Fifty percent inhibitory concentration (IC50) values of gallic acid on the cell viability of SBC-3, EBC-1 and A549 were around 10, 20 and 60 microg/ml, respectively. The IC50 value for SBC-3/CDDP cells was almost the same as that of SBC-3, suggesting that susceptibility of cells to gallic acid-induced apoptosis is not altered by the acquisition of cisplatin resistance. The apoptotic process was effectively triggered by 30 min exposure to gallic acid. A caspase inhibitor and alpha-tocopherol effectively prevented the gallic acid-induced apoptosis, indicating the involvememt of caspase activation and oxidative processes during the course of apoptosis in gallic acid-treated cancer cells. These findings suggest the possible applicability of gallic acid in lung cancer therapy, especially to circumvent resistance to anti-cancer drugs.

Adenocarcinoma↗
PubMedDate not supplied

Changes in amino acid pool and utilization during apoptosis in HL-60 cells induced by epigallocatechin gallate or gallic acid.

Recent studies have demonstrated the apoptosis-inducing potential of epigallocatechin gallate (EGCG), a major component of green tea, against various cultured cell lines. By using an amino acid analyzer, we investigated here the possible changes in the amino acid pool and utilization during the apoptosis of HL-60 cells induced by EGCG or gallic acid, a structural unit of tannin. Sublethal concentrations of EGCG initially elevated and then reduced the intracellular concentrations of most of amino acids except for glutamic acid and aspartic acid, whereas lethal concentrations of EGCG continuously reduced these amino acid pools during 6 hours. Both sublethal and lethal concentrations of gallic acid initially elevated and then reduced these amino acid pools. Both inducers elevated the intracellular accumulation and production of arginine and extensively reduced the utilization of other amino acids. These data demonstrate that EGCG showed more severe effects on the amino acid pool and utilization than gallic acid, which may explain, at least in part, the difference in apoptosis-inducing potential between these inducers.

Amino Acids↗