Gallic acid

Antioxidant and pro-oxidant properties of ascorbic acid and gallic acid[Reference: WebLink]

Food Chem., 2002, 79(3):307-13.

The antioxidant and pro-oxidant properties of ascorbic acid (AA) and Gallic acid (GA) were investigated.
METHODS AND RESULTS:
AA and GA, at a concentration of 1.65 mM, accelerate the oxidation of deoxyribose induced by Fe3+–EDTAJH2O2. The reducing power of these two compounds increased upon increasing the concentration. AA and GA showed no chelating ability toward iron (II). At a concentration of 4.17 mM, AA and GA exhibited 42.1 and 43.9% scavenging effects on DPPH radicals, respectively. They exhibited 60% scavenging effects on hydrogen peroxide at a concentration of 4.17 mM. No toxicity was found in AA and GA toward human lymphocytes. AA, at 0.82 mM, and GA, at 0.6 mM, exhibited the maximal DNA damage, the means of tail DNA% were 14.8 and 28.8%, respectively. When AA and GA were mixed with H2O2, they exhibited a slight inhibitory effect on DNA damage induced by H2O2 on pre-incubating both the compounds with human lymphocytes for 30 min before exposure to H2O2.
CONCLUSIONS:
The antioxidant activities of AA and GA at a higher concentration were mainly due to the scavenging of hydrogen peroxide in this system. The pro-oxidant mechanism for AA and GA acid is most likely due to the strong reducing power and weak metalchelating ability.

Antimelanogenic and antioxidant properties of gallic acid.[Pubmed: 17541153]

Biol Pharm Bull. 2007 Jun;30(6):1052-5.

To find novel skin-whitening agents, the melanogenesis inhibitory action of Gallic acid (GA) was investigated.
METHODS AND RESULTS:
In this current study, the effects of GA on mushroom tyrosinase, tyrosinase inhibitory activity, and melanin content were assessed in B16 melanoma cells (B16 cells). Results indicated that GA has a strong antityrosinase activity (IC50=3.59x10(-6) M). Furthermore, data on murine tyrosinase activity and melanin biosynthesis revealed that GA effectively suppressed murine tyrosinase action and the amount of melanin. To investigate the relation between GA's inhibition of melanogenesis and antioxidant activity, the effect of GA on reactive species (RS) generation and the reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio in were determined in B16 cells. Results indicated that GA effectively down-regulated the RS generation and enhanced the GSH/GSSG ratio.
CONCLUSIONS:
Based on these results, I propose that GA exerts antimelanogenic activity coupled with antioxidant properties by suppressing RS generation and maintaining a higher GSH/GSSG ratio.

Gallic acid inhibits brush border disaccharidases in mammalian intestine.[Reference: WebLink]

Nut. Res., 2007, 27(4):230-5.

Intestinal epithelium constitutes the primary target tissue for interaction with dietary micronutrients. The objective of this study was to determine if Gallic acid, a polyphenol that is an important constituent of various edible plant-based foods, affects brush border disaccharidases in mammalian intestine.
METHODS AND RESULTS:
In this investigation, we found that 0.05 to 0.6 mmol/L Gallic acid inhibited sucrase activity by 34% to 86%. Optimum enzyme inhibition was observed at 0.4-mmol/L Gallic acid concentration, which was 82% in the rat, 83% in LACA/L mice, 50% in BALB/c mice, and 28% in rabbit intestine. The observed enzyme inhibition was reversible in rat intestines. Gallic acid also depressed the activities of maltase (42%), trehalase (45%), and lactase (13%) in the rat. Inhibition of sucrase activity by Gallic acid was mainly between pH 4.8 to 7.2, whereas at alkaline pH (7.7-8.5), Gallic acid stimulated enzyme activity by 20% to 30% in both rat and rabbit intestines. Kinetic analysis revealed that Gallic acid was a fully competitive inhibitor of rat sucrase at pH 5.5 and 6.8. The effect of Gallic acid together with various -SH group–reacting reagents showed that the observed inhibition was additive in nature. Similar results were obtained in the presence of 0.4 mmol/L Gallic acid and 4 mmol/L harmaline, a plant alkaloid.
CONCLUSIONS:
These findings suggest that Gallic acid is a potent inhibitor of brush border sucrase and other disaccharidases and thus could potentially interfere with the digestive functions of the intestine.

Anti-tumor effect of gallic acid on LL-2 lung cancer cells transplanted in mice.[Pubmed: 11707653]

Anticancer Drugs. 2001 Nov;12(10):847-52.

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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.

Radical intensity and cytotoxic activity of curcumin and gallic acid.[Pubmed: 9858929]

Anticancer Res. 1998 Sep-Oct;18(5A):3487-91.

Natural phenolic compounds, curcumin and Gallic acid, were compared for their cytotoxic activity in relation to their radical modulating activity.
METHODS AND RESULTS:
These two compounds induced apoptotic cell death in human promyelocytic leukemic HL-60 cells and human oral squamous carcinoma HSC-4 cells. Curcumin was more cytotoxic than Gallic acid. Catalase reduced significantly the cytotoxic activity of Gallic acid, but not that of curcumin. ESR spectroscopy demonstrated that curcumin produced radicals under alkaline conditions, scavenged the superoxide anion radical, and enhanced the radical intensity of sodium ascorbate at higher concentrations. As compared with curcumin, Gallic acid produced higher amounts of radicals and more efficiently scavenged the superoxide anion radical. Gallic acid reduced the radical intensity of sodium ascorbate, suggesting a possible interaction between these two compounds.
CONCLUSIONS:
These data suggest that curcumin and Gallic acid induce apoptosis by different mechanisms.

Gallic acid, a histone acetyltransferase inhibitor, suppresses β-amyloid neurotoxicity by inhibiting microglial-mediated neuroinflammation.[Pubmed: 22038937]

Mol Nutr Food Res. 2011 Dec;55(12):1798-808.

We examined the biological effect of Gallic acid (GA) as a nuclear factor (NF)-κB acetyltransferase inhibitor on microglial-mediated β-amyloid neurotoxicity and restorative effects on the Aβ-induced cognitive dysfunction.
METHODS AND RESULTS:
The protective effects of GA on the survival of neuronal cells were assessed with an MTT assay and a co-culture system. For the co-culture experiments, both BV-2 and primary microglia cells were treated with GA prior to Aβ stimulation, and conditioned media were transferred to Neuro-2A cells. The mRNA and protein levels of inflammatory cytokines in both microglia and Neuro-2A cells were assessed with real-time polymerase chain reaction and western blotting. Inhibition of nuclear factor kappa B (NF-κB) acetylation with GA treatment resulted in reduced cytokine production in microglia cells and protection of neuronal cells from Aβ-induced neurotoxicity. Furthermore, we observed a restorative effect of GA on Aβ-induced cognitive dysfunction in mice with Y-maze and passive avoidance tests. Finally, we found that GA treatment efficiently blocked neuronal cell death by downregulating the expression of cytokines and the in vivo levels of NF-κB acetylation.
CONCLUSIONS:
These results suggest that selective inhibition of NF-κB acetylation by the histone acetyltransferase inhibitor GA is a possible therapeutic approach for alleviating the inflammatory progression of Alzheimer disease.