Antioxidant Activity Of Tannic Acid Research Articles

Antioxidant Pickering emulsions stabilised by zein/tannic acid colloidal particles with low concentration

SummaryPickering emulsions are widely used as a carrier and protective systems in many fields for encapsulation‐specific bioactive substances. In this current study, we fabricated an antioxidant Pickering emulsions stabilised by zein/tannic acid nanoparticle. Results showed that coalescence and creaming stability of the emulsion highly depended on the concentration of the particles and the zein to TA ratio in the formulation. A 0.3% concentration of zein and a 1:1 zein to TA ratio was found to exhibit optimal stabilising capability. Given the intrinsic antioxidant activity of tannic acid, which forms a protective shell, the oxidative deterioration of the oil in the emulsion could be significantly prevented. These data suggest that the ZTNPs established in the present study are a promising emulsifier in the Pickering emulsion. It is promising as a green, safe, high‐performance particle stabiliser and a novel food ingredient for use in interface‐oriented food systems.

Antioxidant and α-amylase inhibitory activities of tannic acid

Tannic acid widely exists in plants, which forms a part of human diet. The antioxidant activity of tannic acid was evaluated by the chemical and cellular antioxidant assays. And its α-amylase inhibitory activity and behavior were also investigated. It was found that hydrogen- and electron donating capacities of tannic acid were higher than those of tertiary butylhydroquinone (TBHQ) based on reducing power, ABTS and DPPH radical scavenging assays. But for its low hydrophobic property, the antioxidant activity of tannic acid in linoleic acid system was inferior to that of TBHQ. In the cellular antioxidant assay, tannic acid showed the higher activity than gallic acid in the "PBS wash" protocol, which could attribute to its high binding capacity of cell membrane. Compared with acarbose, tannic acid possessed the stronger α-amylase inhibitory capacity. And the static fluorescence quenching of α-amylase in the presence of tannic acid could be also observed, which was caused by their binding interaction.

The Effects of Monosodium Glutamate and Tannic Acid on Adult Rats.

BackgroundMonosodium glutamate (MSG) is a widely-used flavor enhancer and stabilizer in ready-made or packaged foods. The excessive use of MSG has been shown to increase oxidative stress in different organ systems and causes glucose metabolism disorders, obesity, and coronary diseases.ObjectivesIn this study, the antioxidant activity of tannic acid was investigated experimentally with respect to its protective effects against overdosed MSG-induced oxidative stress in rats. The study took place in Turkey in August 2013.MethodsFour groups (n = 7) of three- to four-month-old Sprague-Dawley female rats were used in this study. The first group was the control, who were administered saline. The second group received tannic acid (50 mg/kg, 3 days) intraperitoneally (i.p.). The third group received MSG (2 g/kg, 7 days) i.p., and the fourth group received both tannic acid (50 mg/kg, 3 days, pretreatment) and MSG (2 g/kg, 7 days) i.p. The animals were euthanized ten days later. Blood was collected for determining the hematological values and blood glucose levels. Superoxide dismutase (SOD) and malondialdehyde (MDA) levels were determined in the brain, liver, and kidney homogenates, and in the erythrocyte hemolysate. Histopathological examination of the brain, liver, and kidneys was conducted through hematoxylin-eosin staining.ResultsThe data showed that the tannic acid treatment statistically decreased the MDA levels in the brain tissues of the group administered MSG and tannic acid (P < 0.001) when compared to the corresponding values of the control group. The SOD activities in the blood hemolysates of the MSG and tannic acid group increased when compared to the corresponding values for the MSG group (P < 0.01). Additionally, we found that pretreatment with tannic acid reduced blood glucose levels in comparison to the levels of the MSG group (P = 0.029). The results of our study show that tannic acid pretreatment in adult rats decreased blood glucose levels and oxidative stress.ConclusionsIn the literature, it was observed that short-term MSG exposure does not cause significant histological changes in the kidneys, liver, or brain cortex. These findings should be re-evaluated in additional long-term studies.

Radical scavenging and antioxidant activity of tannic acid

Tannic acid, a naturally occurring plant polyphenol, is composed of a central glucose molecule derivatized at its hydroxyl groups with one or more galloyl residues. In the present paper, we examines the in vitro radical scavenging and antioxidant capacity of tannic acid by using different in vitro analytical methodologies such as 1,1-diphenyl-2-picryl-hydrazyl free radical (DPPH) scavenging, 2,2′-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) radical scavenging activity, total antioxidant activity determination by ferric thiocyanate, total reducing ability determination using by Fe3+–Fe2+ transformation method, superoxide anion radical scavenging by riboflavin–methionine-illuminate system, hydrogen peroxide scavenging and ferrous ions (Fe2+) chelating activities. Also, butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), α-tocopherol and trolox, a water-soluble analogue of tocopherol, were used as the reference antioxidant radical scavenger compounds.Tannic acid inhibited 97.7% lipid peroxidation of linoleic acid emulsion at 15μg/mL concentration. On the other hand, the above mentioned standard antioxidants indicated an inhibition of 92.2%, 99.6%, 84.6% and 95.6% on peroxidation of linoleic acid emulsion at 45μg/mL concentration, respectively. In addition, tannic acid had an effective DPPH scavenging, ABTS+ radical scavenging, superoxide anion radical scavenging, hydrogen peroxide scavenging, Fe3+ reducing power and metal chelating on ferrous ions activities. Also, those various antioxidant activities were compared to BHA, BHT, α-tocopherol and trolox as references antioxidant compounds. The present study shows that tannic acid is the effective natural antioxidant component that can be used as food preservative agents or nutraceuticals.

Tannic acid inhibits in vitro iron-dependent free radical formation

The antioxidant activity of tannic acid (TA), a plant polyphenol claimed to possess antimutagenic and anticarcinogenic activities, was studied by monitoring (i) 2-deoxyribose degradation (a technique for OH detection), (ii) ascorbate oxidation, (iii) ascorbate radical formation (determined by EPR analysis) and (iv) oxygen uptake induced by the system, which comprised Fe(III) complexes (EDTA, nitrilotriacetic acid (NTA) or citrate as co-chelators), ascorbate and oxygen. TA removes Fe(III) from the co-chelators (in the case of EDTA, this removal is slower than with NTA or citrate), forming an iron–TA complex less capable of oxidizing ascorbate into ascorbate radical or mediating 2-deoxyribose degradation. The effectiveness of TA against 2-deoxyribose degradation, ascorbate oxidation and ascorbate radical formation was substantially higher in the presence of iron–NTA (or iron–citrate) than with iron–EDTA, which is consistent with the known formation constants of the iron complexes with the co-chelators. Oxygen uptake and 2-deoxyribose degradation induced by Fe(II) autoxidation were also inhibited by TA. These results indicate that TA inhibits OH formation induced by Fe(III)/ascorbate/O2 mainly by arresting Fe(III)-induced ascorbate oxidation and Fe(II) autoxidation (which generates Fe(II) and H2O2, respectively), thus limiting the production of Fenton reagents and OH formation. We also hypothesize that the Fe(II) complex with TA exhibits an OH trapping activity, which explains the effect of TA on the Fenton reaction.

Anti-oxidant, pro-oxidant properties of tannic acid and its binding to DNA

Tannic acid has numerous food and pharmacological applications. It is an additive in medicinal products, and is used as a flavouring agent and as an anti-oxidant in various foods and beverages. We have previously shown that tannic acid in the presence of Cu(II) causes DNA degradation through generation of reactive oxygen species. On the other hand, it exhibits antimutagenic and anticarcinogenic activities, and induces apoptosis in animal cells. It is known that most plant-derived polyphenolic anti-oxidants also act as pro-oxidants under certain conditions. In this paper, we compare the anti-oxidant and pro-oxidant properties of tannic acid and its structural component gallic acid. It is shown that tannic acid is the most efficient generator of the hydroxyl radical in the presence of Cu(II), as compared with gallic acid and its analogues syringic acid and pyrogallol. The anti-oxidant activity of tannic acid was studied by its effect on hydroxyl radical and singlet oxygen mediated cleavage of plasmid DNA. Again, tannic acid provided the maximum protection against cleavage, while gallic acid and its structural analogues were found to be non-inhibitory or partially inhibitory. The results suggest that the structural features of tannic acid that are important for its anti-oxidant action are also those that contribute to the generation of hydroxyl radicals in the presence of Cu(II). Restriction analysis of treated phage DNA and thermal melting profiles of calf thymus DNA indicated that tannic acid strongly binds to DNA. Indirect evidence indicates that modification of DNA bases may also occur.

Polyphenol tannic acid inhibits hydroxyl radical formation from Fenton reaction by complexing ferrous ions

Tannic acid (TA), a plant polyphenol, has been described as having antimutagenic, anticarcinogenic and antioxidant activities. Since it is a potent chelator of iron ions, we decided to examine if the antioxidant activity of TA is related to its ability to chelate iron ions. The degradation of 2-deoxyribose induced by 6 μM Fe(II) plus 100 μM H 2O 2 was inhibited by TA, with an I 50 value of 13 μM. Tannic acid was over three orders of magnitude more efficient in protecting against 2-deoxyribose degradation than classical ⋅OH scavengers. The antioxidant potency of TA was inversely proportional to Fe(II) concentration, demonstrating a competition between H 2O 2 and AT for reaction with Fe(II). On the other hand, the efficiency of TA was nearly unchanged with increasing concentrations of the ⋅OH detector molecule, 2-deoxyribose. These results indicate that the antioxidant activity of TA is mainly due to iron chelation rather than ⋅OH scavenging. TA also inhibited 2-deoxyribose degradation mediated by Fe(III)-EDTA (iron=50 μM) plus ascorbate. The protective action of TA was significantly higher with 50 μM EDTA than with 500 μM EDTA, suggesting that TA removes Fe(III) from EDTA and forms a complex with iron that cannot induce ⋅OH formation. We also provided evidence that TA forms a stable complex with Fe(II), since excess ferrozine (14 mM) recovered 95–96% of the Fe(II) from 10 μM TA even after a 30-min exposure to 100–500 μM H 2O 2. Addition of Fe(III) to samples containing TA caused the formation of Fe(II) n –TA, complexes, as determined by ferrozine assays, indicating that TA is also capable of reducing Fe(III) ions. We propose that when Fe(II) is complexed to TA, it is unable to participate in Fenton reactions and mediate ⋅OH formation. The antimutagenic and anticarcinogenic activity of TA, described elsewhere, may be explained (at least in part) by its capacity to prevent Fenton reactions.