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At least 19 recordsLinked to original sources
PubMed2000

Inhibition of xanthine oxidase and suppression of intracellular reactive oxygen species in HL-60 cells by theaflavin-3,3'-digallate, (-)-epigallocatechin-3-gallate, and propyl gallate.

The inhibitory effects of five tea polyphenols, namely theaflavin (TF1), theaflavin-3-gallate (TF2), theaflavin-3,3'-digallate (TF3), (-)-epigallocatechin-3-gallate (EGCG), and gallic acid, and propyl gallate (PG) on xanthine oxidase (XO) were investigated. These six antioxidant compounds reduce oxidative stress. Theaflavins and EGCG inhibit XO to produce uric acid and also act as scanvengers of superoxide. TF3 acts as a competitive inhibitor and is the most potent inhibitor of XO among these compounds. Tea polyphenols and PG all have potent inhibitory effects (>50%) on PMA-stimulated superoxide production at 20 approximately 50 microM in HL-60 cells. Gallic acid (GA) showed no inhibition under the same conditions. At 10 microM, only EGCG, TF3, and PG showed significant inhibition with potency of PG > EGCG > TF3. The superoxide scavenging abilities of these six compunds are as follows: EGCG > TF2 > TF1 > GA > TF3 > PG. PG was the most potent inhibitor of PMA-stimulated H(2)O(2) production in HL-60 cells. The order of H(2)O(2) scavenging ability was TF2 > TF3 > TF1 > EGCG > PG > GA. Therefore, the antioxidative activity of tea polyphenols and PG is due not only to their ability to scavenge superoxides but also to their ability to block XO and related oxidative signal transducers.

Antioxidants↗
PubMed1981

[Effect of propyl gallate on the antibacterial activity of meclocycline sulfosalicylate].

Propyl gallate shows little antibacterial activity however it markedly potentiates the activity of meclocycline against Pseudomonas, Proteus, Serratia, Escherichia coli and Klebsiella strains. The potentiating effect of propyl gallate is seen especially with resistant strains whereas sensitive strains of Salmonella do not manifest a potentiating effect on meclocycline by propyl gallate. The mechanism of action of propyl gallate is discussed.

Bacteria↗
PubMed1980

Enhancing and inhibiting effects of propyl gallate on carcinogen-induced mutagenesis.

The food additive propyl gallate has a significant effect on the mutagenic activities of several carcinogens as measured by the Salmonella/microsome mutagenesis assay. Propyl gallate (10(-2) to 10(-4) M) inhibits the mutagenic activites of the carcinogens N-methyl-N-'nitro-N-nitrosoguanidine (MNNG) and N-acetoxy-2-acetylaminofluorene (N-acetoxy-AAF). It also reduces the mutagenic effect of aflatoxin B1, a carcinogen which requires activation with a S-9 microsomal preparation. In contrast, propyl gallate at equimolar concentrations causes an enhancement of the mutagenic activities of the carcinogens N-hydroxy-2-acetylaminofluorene (N-hydroxy-AAF) and 4-nitroquinoline 1-oxide (4NQO). The enhancement of 4NQO-induced mutagenesis occurs with a range of 4NQO concentrations. Moreover, both frameshift (TA98) and base substitution (TA100) bacteria indicator strains demonstrate an enhanced mutagenesis to 4NQO in the presence of the propyl-gallate. Propylgallate alone has no effect on the spontaneous reversion rate of S. typhimurium to histidine propotrophy.

Biotransformation↗
PubMed1990

Allergic contact dermatitis from propyl gallate: dose response comparison using various application methods.

The antioxidant propyl gallate, in a deodorant product, caused an allergic contact dermatitis in 1 subject during developmental controlled use testing. Subsequent dose response elicitation studies with this subject revealed a differing threshold of sensitivity to propyl gallate dependent upon application method. Increasing the level of occlusion increased the elicitation response. Responsiveness from greatest to least was: occluded patch on the upper arm greater than semi-occluded axilla greater than open application on the antecubital fossa. The thresholds determined for propyl gallate (w/v in 25:75 ethanol:water) were: (a) 0.0025% for the upper arm occluded patch; (b) 0.0035% for the underarm without shaving; (c) 0.005% for the underarm with shaving; (d) 0.015% for the antecubital fossa. Occluded patch responsiveness to propyl gallate was monitored and remained unchanged throughout a 2-year period. These data are useful in understanding the relationship between occlusive allergic contact dermatitis patch testing and clinical contact dermatitis.

Administration, Cutaneous↗
PubMed1994

Propyl gallate as a hepatoprotector in vitro and in vivo.

Recently, there has been renewed interest in propyl gallate, a preservative in foods and fuels. This compound, which exhibits antimicrobial activity, has been found to be toxicologically safe after almost 30 years of evaluation. In the present study, we examined whether propyl gallate is a hepatoprotective antioxidant, and investigated some of its bases of action vis-à-vis Trolox, a vitamin E analogue. In isolated rat hepatocytes, propyl gallate prolonged substantially cell survival against oxyradicals generated with xanthine oxidase-hypoxanthine. The protection was dose dependent and excelled that of Trolox, mannitol, or ascorbate, each at or near its optimum level in the same system. In rats undergoing an 80-min partial hepatic ischemia, infusion of propyl gallate at 20 mumol/kg body weight just before a 24-hr reperfusion salvaged the organ by 80.0 +/- 11.5%, an extent comparable to that with Trolox. Mechanistically, we found that propyl gallate (a) protected hepatocytes against the cascade of oxyradicals produced by xanthine oxidase-hypoxanthine; (b) protected hepatocytes against superoxide radicals generated specifically by menadione; (c) protected the functionally important hepatic vascular endothelial cells more effectively than Trolox against xanthine oxidase-hypoxanthine, and (d) approximately halved the amount of lipid conjugated dienes (a more specific marker of oxyradical damage than malondialdehyde) formed in tissues after oxidant damage. Therefore, there are fundamental reasons why propyl gallate is an effective antioxidant-based hepatoprotector, both in vitro and in vivo.

Animals↗
PubMedDate not supplied

No evidence of carcinogenicity of D-mannitol and propyl gallate in F344 rats or B6C3F1 mice.

Chronic toxicity and carcinogenicity studies were conducted on D-mannitol and propyl gallate in F344 rats and B6C3F1 mice. Groups of 50 rats and 50 mice of each sex were maintained on diets containing either 0, 2.5 or 5.0% D-mannitol or 0, 0.6 or 1.2% propyl gallate for 103 wk. D-Mannitol had no effect on survival or mean body weight of rats and mice, and feed consumption was approximately the same in control and treated groups in each species. Gastric fundal gland dilation occurred at a higher incidence in treated female rats than in controls. A mild nephrosis characterized by focal vacuolization of the renal tubular epithelium was observed in an increased incidence in treated mice. No significant increase in tumour incidence was observed in any of the treated groups in comparison with the corresponding controls. Survival of rats and mice given propyl gallate was similar to that of the controls. Mean body weights were lower in chemically exposed animals, and more so for females. Male rats exposed to propyl gallate showed an increased incidence of hepatic cytoplasmic vacuolization and suppurative inflammation of the prostate gland. Tumours of the preputial gland, islet-cell tumours of the pancreas, and phaeochromocytoma of the adrenal gland occurred at a significantly (P less than 0.05) higher incidence in the low-dose male rats. Malignant lymphoma occurred with a positive trend in male mice (control 1/50, low dose 3/49 and high dose 8/50), and the incidence in the high-dose group was significantly (P less than 0.05) higher than in the control group. However, since the incidence in the control group was much less than the historical control rate (36/398 or 9%) in this laboratory, this apparent increase was not considered to be related to propyl gallate administration. Under the conditions of these studies, neither D-mannitol nor propyl gallate was considered to be carcinogenic to F344 rats or B6C3F1 mice of either sex.

Administration, Oral↗
PubMed1996

Gender specific alterations in antioxidant status of aging Zaprionus paravittiger fed on propyl gallate.

Zaprionus paravittiger fed on propyl gallate (PG) supplemented diet (2.5, 25 and 250 micrograms/ml) showed an increase in life span. Further increase in concentration (2500, 5000 and 7500 micrograms/ml) accelerated the mortality rate. Females exhibited longer life span as compared to males. Antioxidant enzymes (catalase, peroxidase and glutathione reductase) were measured in control and optimum concentration of PG (25 micrograms/ml) fed flies at various age intervals. Antioxidant enzyme activities showed an increase during reproductive phase. Catalase and glutathione reductase activities decreased with age however no significant change was observed in peroxidase activity. The females exhibited higher enzyme activities as compared to males in control and PG fed group at most of the age intervals. PG feeding caused a significant increase in catalase and glutathione reductase activities in both the sexes. These findings suggest the PG has dose dependent and sex specific influence on longevity of Z. paravittiger and support the view that longevity and activity of antioxidant enzymes are positively linked.

Aging↗
PubMed1998

DNA strand break induction and enhanced cytotoxicity of propyl gallate in the presence of copper(II).

The antioxidant propyl gallate (PG) induced single strand breaks in PM2 DNA at concentrations higher than 0.25 microM when it was combined with copper concentrations at 5 microM and above. In combination with 100 microM CuCl2, extensive double strand breakage was also observed. Neither PG alone nor CuCl2 showed any strand breaking properties. DNA strand breakage was inhibited by addition of catalase or the Cu(I) chelator neocuproine, indicating the involvement of H2O2 and a Cu(II)/Cu(I) redox cycle in the DNA damage. DNA damage of PG/Cu(II) was also observed in human fibroblasts. Using the alkaline elution technique concentrations of 0.15-0.5 mM PG induced DNA strand breaks in combination with 2.5 mM CuCl2, while the single substances did not show any effect. At these concentrations cell viability measured by the MTT assay was not reduced by more than 10%; however, cell growth was inhibited by PG in combination with Cu(II). This growth inhibition was apparently due to the DNA damage incurred by PG/Cu(II). The synergistic interaction between PG and Cu(II) is probably caused by a redox reaction between both compounds, whereby reactive species such as ROS are formed, which are responsible for the observed genotoxic and cytotoxic effects. Our results demonstrate that the antioxidative and cytoprotective properties of propyl gallate may change to prooxidative, cytotoxic and genotoxic properties in the presence of Cu(II).

Catalase↗
PubMed1987

Evidence for the addition of the superoxide anion to the anti-oxidant n-propyl gallate in aqueous solution.

n-Propyl gallate reacts with the superoxide radical anion in aqueous solution (k = 5.1 x 10(5) mol-1 dm3 s-1). The spectrum of the transient species so formed has been measured (absorbance maximum at 550 nm, epsilon = 1360 mol-1 dm3 cm-1). Electron or H atom transfer processes as well as proton abstraction have been excluded as possible mechanisms, and it is proposed that an addition reaction takes place.

Antioxidants↗
PubMed1985

Protective actions of propyl gallate, a lipoxygenase inhibitor, on the ischemic myocardium.

Products of the lipoxygenase pathway of arachidonate metabolism, including hydroperoxides, free radicals, and leukotrienes, are thought to mediate ischemic damage during acute myocardial ischemia (MI). Propyl gallate (1 mg/kg/h) was infused in anesthetized cats 0.5 h after coronary artery occlusion. Propyl gallate did not influence mean arterial blood pressure (MABP), heart rate (HR), or the product of these, the pressure-rate index. Treatment of MI with propyl gallate significantly reduced the plasma accumulation of creatine kinase (CK). This was confirmed by reduced CK loss in biopsies from the ischemic region of the heart, indicative of a protective effect. Propyl gallate also reduced the loss of compounds containing amino-nitrogen groups from the ischemic region, although it did not significantly reverse the S-T segment elevation in the electrocardiogram. These results are consistent with the concept that inhibition of formation of lipoxygenase products protects the myocardium from ischemic damage. This study also helps explain the work of others demonstrating that combined cyclooxygenase-lipoxygenase inhibitors or depletion of leukocytes is beneficial in MI.

Animals↗
PubMed1992

Propyl gallate on liposomes.

A hypothesis suggesting that the allergic potential of propyl gallate is boosted by its attachment to liposomes in cosmetics is put forward. 13 women with allergy to propyl gallate are presented.

Adult↗
PubMed1976

The local antinociceptive and topical anti-inflammatory effects of propyl gallate in rodents.

1 In common with several anti-inflammatory, analgesic, local anaesthetic and antioxidant drugs, propyl gallate in vitro inhibited the biosynthesis of prostaglandin E2 and F2alpha from arachidonic acid by a prostaglandin synthetase from bull seminal vesicles. 2 In common with analgesic drugs, propyl gallate reduced the ability of arachidonic acid, acetylcholine or acetic acid to cause abdominal constriction in mice. 3 Using a new method for evaluating anti-inflammatory activity, we demonstrated the effectiveness of aspirin or indomethacin given subcuteneously before u.v. irradiation of guinea-pig ears, the prophylactic action of topically applied sunscreen agents and the therapeutic value of bufexamac and propyl gallate applied after irradiation.

Abdomen↗
PubMed1980

[Influence of propyl-gallate and 2-mercaptopropionylglycine on the development of acute inflammatory reactions and on biosynthesis of PGE2].

Anti-inflammatory activity of Propyl Gallate and 2.mercaptopropionylglycine, administered intraperitoneally to the rat, was evaluated against paw edema induced by Carrageenan, Bradykinin, Serotonin and Dextran. In addition, the influence of these chemicals on PGE2 formation from added arachidonic acid to spleen microsomal fraction incubated "in vitro" was assayed. Our results indicate Propyl Gallate and 2.mercaptopropionylglycine depress significantly the development of acute inflammatory reactions provoked by the above mentioned phlogogens and are able to limit the biosynthesis of PGE2. The last inhibitory activity appears to be less potent than that exerted by some non-steroidal anti-inflammatory agents, namely Indomethacin and Oxametacine, which act primarily by interfering with cyclo-oxigenase activity. In our opinion, the anti-inflammatory effect of Propyl Gallate and 2.mercaptopropionylglycine might be dependent on both the scavenger properties of the two compounds against some final products of lipid peroxides (aldehydes) originated at the inflammation site and the partial inhibition of the formation of PGE2 by acting on the cyclo-oxigenase system.

Amino Acids, Sulfur↗
PubMed1982

Transfer of radiation-induced spins from deoxyribonucleic and thymidylic acids to propyl gallate.

When calf thymus deoxyribonucleic acid (DNA), propyl gallate (PG) and their five molecular mixtures (with PG content of 1, 2, 5, 10 and 20%) are irradiated with gamma-rays in dry state in vacuum at 296 degrees K, the ESR spectra of all molecular mixtures differ strikingly from those of DNA, but bear a close resemblance to those of PG. The spin yield in the PG contained in these mixtures is two to three orders of magnitude higher than that in the case of PG irradiated separately. Furthermore, on the basis of the relative saturation characteristics of ESR spectra, these molecular mixtures behave more like PG than like DNA. It may be inferred that the radiation-induced spins could be transferred from DNA to PG. With r representing the molar ratio of nucleotides to PG, we have found a good linear correlation between the transfer ratio (TR) and square root of r. One PG molecule could protect at least 68 nucleotides in the duplex DNA chain, and thereby the minimal range of spin transfer is estimated at 115 A. Results obtained from irradiation at 77 degrees K show that PG exerts no protective effect on DNA, so DNA sustains an irreversible damage. It is thought that the spin transfer from DNA to PG is exclusively due to a hydrogen transfer mechanism. We have also demonstrated the transfer of radiation-induced spins from both thermally denatured DNA and TMP to PG. The former process can be ascribed primarily to the hydrogen transfer mechanism, whereas the latter, as in the case of native DNA, exclusively to this mechanism.

Animals↗
PubMed1999

Induction of lipid peroxidation in human fibroblasts by the antioxidant propyl gallate in combination with copper(II).

The antioxidant propyl gallate (PG) induced lipid peroxidation in combination with non-toxic Cu(II) concentrations in human fibroblasts. This was measured by the thiobarbituric acid assay (TBA assay) and by detection of accumulating fluorescent products after a 1-h treatment of cells with CuCl2/PG at concentrations higher than 0.125 mM. PG alone led to a significant reduction of thiobarbituric acid-reactive substances (TBARS) demonstrating its antioxidative properties. Time course studies of lipid peroxidation by PG/Cu(II) showed that formation of TBARS was preceded by a lag phase of 60 min. Thereafter, the TBARS value increased rapidly for 1 h and then reached a constant maximum or slightly decreased. The induction of lipid peroxidation by PG/Cu(II) is probably due to the formation of reactive species like reactive oxygen species (ROS), Cu(I) and semiquinone radicals which are able to participate in initiation and propagation of lipid peroxidation. Combination effects of PG/Cu(II) were demonstrated also on inhibition of membrane-bound succinate dehydrogenase. Cytosolic esterases were affected only slightly. The greater susceptibility of membrane-bound enzymes is in accordance with the lipid peroxidation-inducing effects of PG/Cu(II).

Antioxidants↗
PubMed1995

Attenuation of reperfusion injury by the antioxidant n-propyl gallate.

We studied the effects of n-propyl gallate (n-PG) on Langendorff preparations of isolated rat hearts. Perfusion of the hearts with Krebs-Henseleit (KH) solution containing 20 microM n-PG did not cause a statistically significant change in either left ventricular systolic pressure (LVSP), end-diastolic pressure (LVEDP), developed pressure (LVDP), or heart rate (HR), indicating that n-PG has little acute myocardial toxicity. The effects of n-PG on the reperfused and ischemic myocardium were tested in hearts subjected to 15-min global P4 the ischemic hearts with KH buffer resulted in the recovery of the LVDP to 66 +/- 7% (mean +/- SEM, n = 11) and the recovery of the rate-pressure product (RPP) to 65 +/- 7% of their preischemic values. The LVEDP of the reperfused hearts was 30 +/- 5 mm Hg as compared with the preischemic LVEDP of 5.2 +/- 0.9 mm Hg. The difference between the coronary flow rate of the preischemic hearts (15.4 +/- 0.8 ml/min) and the reperfused hearts (13.9 +/- 0.9 ml/min) was not statistically significant (p > 0.05). Addition of n-PG, at the time of reperfusion, resulted in with KH buffer containing 20 microM n-PG had LVEDP of 6.2 +/- 0.4 mm Hg, and both LVDP and RPP recovered to 92 +/- 4% of the preischemic control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗