Regeneration Of Tocopherol Research Articles

Enhancing the oxidation stability and bioaccessibility of algal oil emulsion by using tocopherol and chlorogenic acid

The effects of tocopherol and chlorogenic acid on the oxidation stability and bioaccessibility of algal oil emulsion were investigated. The results showed that the compound antioxidant (300 ppm tocopherol + 200 ppm chlorogenic acid) could effectively inhibit the oxidation of algal oil emulsion. Based on the changes in antioxidant content during storage and their distribution at the interface, it is speculated that the interaction mechanism between tocopherol and chlorogenic acid is that chlorogenic acid promotes the regeneration of tocopherol and alters their distribution at the interface through their interaction. The calculation result of FMO showed that the ΔE of chlorogenic acid (4.0456 eV) is smaller than that of α-tocopherol (6.4823 eV), indicating a stronger electron-donating capacity, which further validated the mechanism of the interaction between tocopherol and chlorogenic acid. The compound antioxidant had no significant effect on the physical stability of the emulsion, and was conducive to improving the bioaccessibility of DHA. These findings provide direction for the design of high oxidation stability functional emulsion systems and valuable ideas for the creation of natural antioxidant combinations.

Zeaxanthin Combined with Tocopherol to Improve the Oxidative Stability of Chicken Oil.

Chicken oil is prone to oxidation due to the high content of unsaturated fatty acids. The interaction of antioxidants was affected by their concentration, ratio, and reaction system. In this article, mixtures of zeaxanthin and tocopherols (α-tocopherol and γ-tocopherol) were chosen to enhance the oxidative stability of chicken oil. The antioxidation of zeaxanthin with tocopherols was analyzed using the Rancimat test, the free radical scavenging capacity and the Schaal oven test (the variation of antioxidant content, PV and shelf life prediction). The optimal concentration of zeaxanthin determined by Rancimat in chicken oil was 20 mg/kg. The binary mixtures have a strong synergistic effect in the ABTS experiment, and the clearance rate was up to 99%, but antagonistic effect in ORAC. The degree of synergism between zeaxanthin and tocopherols was determined by ratio. The interaction between zeaxanthin and α-tocopherol was synergistic, while the types of interaction between zeaxanthin and γ-tocopherol were affected by concentration. The main synergistic interaction mechanism was the regeneration of tocopherol by zeaxanthin. Synergistic combinations of zeaxanthin with α-tocopherol and γ-tocopherol played a key role in the primary oxidation stage of the lipid. The best synergistic combination was A3 (zeaxanthin+α-tocopherol: 15+50 23 mg/kg), which could extend the shelf life of chicken oil (92.46 d) to 146.93 days. This work provides a reference for zeaxanthin and tocopherol to improve the oxidative stability of animal fat.

Preclinical and Clinical Role of Coenzyme Q10 Supplementation in Various Pathological States.

Coenzyme Q10 (CoQ10) is an efficient antioxidant produced endogenously in a living organism. It acts as an important cofactor in the electron transport system of mitochondria and reported as a safe supplement in humans and animals with minimal adverse effect. CoQ10 is found naturally, as a trans configuration, chemical nomenclature of which is 2,3- dimethoxy-5- methyl-6-decaprenyle -1,4-benzoquinone. It is found in the body in two forms. In quinone form (oxidized form), it serves as an electron transporter that transfers the electrons in the electron transport chain between various complexes, and in ubiquinol form (reduced form), it serves as potent antioxidants by scavenging free radicals or by tocopherol regeneration in the living organism. Its primary roles include synthesis of adenosine triphosphate (ATP), stabilizes lipid membrane, antioxidant activity, cell growth stimulation, and cell death inhibition. CoQ10 has shown a variety of pharmacological and clinical effects including neuroprotective, hepatoprotective, anti-atherosclerotic, anticonvulsant, antidepressant, anti-inflammatory, antinociceptive, cardiovascular, antimicrobial, immunomodulatory, and various effects on the central nervous system. Present review has set about to bring updated information regarding to clinical and preclinical activities of CoQ10, which may be helpful to researchers to explore a new bioactive molecules for various therapeutic application.

Kinetic Study of the Tocopherol Regeneration Reaction by Biological Hydroquinones in Micellar Solution

The rate constants (kr) of the regeneration reaction of 7-t-butyl-5-isopropyltocopheroxyl with ubiquinol-10 (UQ10H2), ubiquinol-0 (UQ0H2), alpha-, beta-, and gamma-tocopherolhydroquinones (alpha-, beta-, gamma-TQH2), 2,3,5-trimethyl-1,4-hydroquinone (TMQH2), vitamin K3 hydroquinone (VK3H2), and vitamin C (Vit C) have been measured in 2-propanol/water and micellar solutions by a stopped-flow spectrophotometer. The kr values of these hydroquinones (HQs) in micellar solution remained constant at pHs of 6-9 and increased rapidly by increasing the pH value. The kr values decreased in the order of VK3H2 > gamma-TQH2 > or = alpha-TQH2 > beta-TQH2 > or = UQ10H2 > or = TMQH2 > UQ0H2 >> Vit C at pHs of 6-9. These HQs are dibasic acids and can exist in three different molecular forms, depending on pH. By comparing the kr values with the mole fraction of each molecular form of the HQs, the reaction rate kr1 for the undissociated form, kr2 for the monoanion, and kr3 for the dianion and the pKa1 and pKa2 values were determined. It has been found that the kr values of UQ10H2, alpha-TQH2, beta-TQH2, and gamma-TQH2 (plastoquinol model) are 460, 1430, 494, and 1530 times larger than that of Vit C at pH 7.0, respectively, although the values are similar to that of Vit C in 2-propanol/water. The biological HQs and Vit C coexist in many tissues of animals and plants, and thus, the relative antioxidant activities of HQs and Vit C have been tentatively discussed based on the products of kr values by concentrations in several tissues. The results suggest that these HQs show high activity for the tocopherol regeneration in biological systems.

Effects of menopause and tibolone on antioxidants in postmenopausal women

Oxidative stress has been implicated in the pathogenesis of ageing and menopause, and can arise through the increased production of lipid peroxides and/or a deficiency of antioxidant defence. To investigate the effects of the menopause and tibolone treatment (2.5 mg/day for six months) on plasma antioxidants and lipid peroxidation. Plasma concentrations of ascorbic acid, alpha-tocopherol, total thiol groups, caeruloplasmin, erythrocyte glutathione (GSH) and malondialdehyde (MDA) were measured in 24 postmenopausal and 24 premenopausal healthy women. Data analysis indicates a significant decrease in plasma ascorbic acid, alpha-tocopherol, total thiol groups, [corrected]erythrocyte GSH and a significant increase in lipid peroxides (expressed as MDA concentrations) in postmenopausal women. There was no significant difference between control and study groups in the mean plasma caeruloplasmin concentrations. It was found that there is a significant increase in alpha-tocopherol and significant decrease in lipid peroxide concentrations in postmenopausal after tibolone treatment. The menopause is associated with an increase in oxidative stress and a decrease of some antioxidants, such as ascorbic acid, alpha-tocopherol, total thiols and erythrocyte GSH. Tibolone treatment leads to a decrease in concentrations of plasma lipid peroxide, probably by stimulating direct and indirect mechanisms of tocopherol regeneration and increasing plasma concentrations of vitamin E. However, due to the relatively small numbers involved this study can be regarded as a pilot. Further studies performed on a larger scale are necessary to establish the exact mechanisms of tibolone in inhibiting oxidative stress in postmenopausal women.

Biological functions and metabolic fate of vitamin E revisited.

Information accumulated lately has confirmed the essentiality of vitamin E for humans and provided a better understanding of its biological function and metabolic fate. The discovery of alpha-tocopherol transfer protein, which preferentially binds to RRR-alpha-tocopherol, not only provides conclusive evidence of the essentiality of vitamin E for humans, but also sheds light on the superiority of RRR-alpha-tocopherol biologically over other isomers. The presence of tocopherol regeneration systems and multiple interdependent antioxidant systems is largely responsible for the lack of a widespread deficiency in humans and the difficulty to deplete vitamin E in the adult. The bulk of excess tocopherols consumed is excreted to feces unchanged or to urine with the side chain shortened but the chroman ring intact. The ability of dietary vitamin E to mediate mitochondrial superoxide generation affords a possible mode of action of vitamin E at the tissue levels. By decreasing the generation and/or the levels of reactive oxygen/nitrogen species, dietary vitamin E not only protects against oxidative damage, but also modulates the expression and/or activation of redox-sensitive biological response modifiers that regulate important cellular events.

Changes in antioxidant and pigment pool dimensions in UV-B irradiated maize seedlings

Ultraviolet-B (UV-B) radiation (280–320 nm) is an environmental challenge affecting a number of metabolic functions through the generation of reactive oxygen species (ROS). Plants protect themselves from this harmful radiation by synthesizing flavonoids, which act as a screen inside the epidermal cell layer, and by making adjustments to the antioxidant systems at both cell and whole organism level. This study describes the flavonoid content, the photosynthetic pigment composition and the proline, tocopherol and ascorbate content in UV-B exposed maize plants. Following exposure, the tocopherol content was slightly, but significantly lower, pointing to the membrane environment as a primary target for UV-B radiation. The water-soluble antioxidant content was largely unaffected, but an enhanced turnover in the ascorbate–glutathione cycle might be needed for tocopherol regeneration.

Ascorbate and glutathione metabolism in two sunflower cell lines of differing α-tocopherol biosynthetic capability

The natural antioxidants, tocopherols and ascorbate (ASC), are of great interest in terms of human health, because of their role in the prevention of chronic diseases. In cell metabolism, tocopherols are the major lipid-soluble antioxidants, whereas ASC and glutathione (GSH) are hydro-soluble antioxidants. These three metabolites cooperate in scavenging for oxygen radicals and protecting cell membranes. ASC and GSH are required in the process of regeneration of tocopherol from its α-cromanoxyl radical, while, GSH donates electrons for the reduction of dehydroascorbate (DHA), the fully oxidised form of ASC. Two cell lines of sunflower ( Helianthus annuus L. cv Gloriasol) with differing capability to synthesise α-tocopherol were identified. In spite of the differing content of α-tocopherol (almost threefold higher in the high synthesising cell line, HT, than in the low synthesising one, LT), the cell lines have comparable growth curves. In the cells collected in the stationary phase, the ASC and GSH pools are also significantly higher in the HT cells than in the LT cells. On the other hand, the enzymes responsible for H 2O 2 scavenging and ASC and GSH recycling had higher activity in the LT than in the HT cells. The cooperation between the three antioxidant systems in the maintenance of the cellular redox balance is discussed, as well as the possible utilisation of the HT cell line for the in vitro production of natural antioxidants.

Copper-induced peroxidation of liposomal palmitoyllinoleoylphosphatidylcholine (PLPC), effect of antioxidants and its dependence on the oxidative stress

In an attempt to deepen our understanding of the mechanisms responsible for lipoprotein peroxidation, we have studied the kinetics of copper-induced peroxidation of the polyunsaturated fatty acid residues in model membranes (small, unilamellar liposomes) composed of palmitoyllinoleoylphosphatidylcholine (PLPC). Liposomes were prepared by sonication and exposed to CuCl 2 in the absence or presence of naturally occurring reductants (ascorbic acid (AA) and/or α-tocopherol (Toc)) and/or a Cu(I) chelator (bathocuproinedisulfonic acid (BC) or neocuproine (NC)). The resultant oxidation process was monitored by recording the time-dependence of the absorbance at several wavelengths. The observed results reveal that copper-induced peroxidation of PLPC is very slow even at relatively high copper concentrations, but occurs rapidly in the presence of ascorbate, even at sub-micromolar copper concentrations. When added from an ethanolic solution, tocopherol had similar pro-oxidative effects, whereas when introduced into the liposomes by co-sonication tocopherol exhibited a marked antioxidative effect. Under the latter conditions, ascorbate inhibited peroxidation of the tocopherol-containing bilayers possibly by regeneration of tocopherol. Similarly, both ascorbate and tocopherol exhibit antioxidative potency when the PLPC liposomes are exposed to the high oxidative stress imposed by chelated copper, which is more redox-active than free copper. The biological significance of these results has yet to be evaluated.

The antioxidant role of α-tocopherol in polymers II. Melt stabilising effect in polypropylene

The antioxidant efficiency of the biological antioxidant α-tocopherol during melt extrusion of polypropylene (PP) was investigated. The melt stabilising effect of α-tocopherol was found to be much higher than that of the commercial synthetic hindered phenol antioxidant Irganox 1010 especially at very low concentrations. The excellent stabilising performance of α-tocopherol was maintained even under severe extrusion conditions. The colour stability of PP processed in the presence of α-tocopherol was shown to be as good as that of Irganox 1010 when the former was used at low concentrations. However, higher concentrations of α-tocopherol imparted greater discoloration to the polymer than Irganox 1010 examined at the same concentrations. The incorporation of a phosphite antioxidant or a polyhydric alcohol (non-antioxidant) was shown to reduce drastically polymer discolouration concomitant with higher levels of retention of the tocopherol in the polymer. This was attributed partly to the reduction of the overall concentration of transformation products, formed from tocopherol as a result of its antioxidant function, and partly to interactions of the co-additives with coloured transformation products and regeneration of tocopherol. The transformation products were shown to be more coloured than the parent antioxidant. A mechanism is proposed for the co-operative interactions between α-tocopherol and phosphite U-626 which result in the improvement in melt stability and reduction in colour of PP.

Regeneration of vitamin E in rat polymorphonuclear leucocytes

The objectives of this study were to determine whether the recycling of tocopherol occurs in elicited rat polymorphonuclear leukocytes and if so, whether the recycling process is anzymic or chemical. When incubated with hemoglobin. tocopherol was oxidized in cell homogenates in a time-and concentration-dependent manner. The oxidized tocopherol could be regenerated by addition of ascorbate, glutathione or nordihydroguaiaretic acid. Time course studies showed a rapid regeneration of tocopherol which peaked at 1 min after the addition of reductants. Determination of the regeneration reaction in the presence of CHCl 3 and MeOH indicated that under these enzyme-denaturing conditions, a considerable amount of tocopherol was still regenerated, suggesting that the regeneration reaction is predominantly a chemical reaction. This study provided direct evidence from mass analysis that oxidized vitamin E can be regenerated by cellular water-soluble reductants such as ascorbate and glutathione.

Regeneration of vitamin E in human platelets.

Human platelets possess active lipoxygenase and cyclooxygenase which convert arachidonic acid to (12S)-12-hydroperoxy-5,8,10,14-eicosatetraenoic acid (12-HPETE) plus (12S)-12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE) and thromboxane B2 plus 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT), respectively. When platelet homogenates were incubated with arachidonate, there was a rapid consumption of platelet tocopherol. Time course analysis revealed that within 0.5 min, over half of arachidonate and tocopherol were metabolized. Mass formation of 12-HPETE and 12-HETE or thromboxane B2 and HHT exceeded that of the mass of tocopherol oxidized. Preincubation with the lipoxygenase inhibitor 5,8,11,14-eicosatetraynoic acid (ETYA) completely abolished this arachidonate-induced tocopherol oxidation whereas cyclooxygenase inhibitors (indomethacin and aspirin) further potentiated tocopherol oxidation, indicating that this oxidation is closely linked with platelet 12-lipoxygenase activity. Incubation with lipoxygenase metabolites of arachidonic acid showed that only 12-HPETE caused a rapid tocopherol oxidation which was followed by a gradual tocopherol regeneration. By using nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor which is also a strong reductant, over 60% of the arachidonate-induced oxidized tocopherol was regenerated. Tocopherol regeneration declined with increasing oxidation time induced by arachidonate, and after 30-60 min virtually no regeneration could be observed, suggesting that the precursor molecule was unstable. We postulate that the precursor molecule is the tocopheroxyl radical. In the presence of ETYA, a lipoxygenase inhibitor without antioxidant properties, either ascorbate or GSH provided significant tocopherol regeneration. Kinetic studies showed that tocopherol regeneration after the addition of ascorbate was essentially completed by 1 min. By contrast, GSH addition caused a steady increase in tocopherol which peaked after 10 min of its addition. To determine whether this rapid regeneration is chemical or enzymic, regeneration was studied in the presence of chloroform and methanol. Comparison of various reductants in this denaturing condition for enzymes showed that ascorbate and NDGA afforded significant regeneration whereas GSH was ineffective, indicating that there are distinct enzymic and non-enzymic mechanisms for tocopherol regeneration. This study provides direct evidence from mass analysis that tocopherol can be regenerated in human cell homogenates. This finding implies that maintenance of membrane tocopherol status may be an essential function of ascorbate and GSH which operate in concert to ensure maximum membrane protection against oxidative damage.

Regeneration of vitamin E in human platelets

Human platelets possess active lipoxygenase and cyclooxygenase which convert arachidonic acid to (12S)-12-hydroperoxy-5,8,10,14-eicosatetraenoic acid (12-HPETE) plus (12S)-12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE) and thromboxane B2 plus 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT), respectively. When platelet homogenates were incubated with arachidonate, there was a rapid consumption of platelet tocopherol. Time course analysis revealed that within 0.5 min, over half of arachidonate and tocopherol were metabolized. Mass formation of 12-HPETE and 12-HETE or thromboxane B2 and HHT exceeded that of the mass of tocopherol oxidized. Preincubation with the lipoxygenase inhibitor 5,8,11,14-eicosatetraynoic acid (ETYA) completely abolished this arachidonate-induced tocopherol oxidation whereas cyclooxygenase inhibitors (indomethacin and aspirin) further potentiated tocopherol oxidation, indicating that this oxidation is closely linked with platelet 12-lipoxygenase activity. Incubation with lipoxygenase metabolites of arachidonic acid showed that only 12-HPETE caused a rapid tocopherol oxidation which was followed by a gradual tocopherol regeneration. By using nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor which is also a strong reductant, over 60% of the arachidonate-induced oxidized tocopherol was regenerated. Tocopherol regeneration declined with increasing oxidation time induced by arachidonate, and after 30-60 min virtually no regeneration could be observed, suggesting that the precursor molecule was unstable. We postulate that the precursor molecule is the tocopheroxyl radical. In the presence of ETYA, a lipoxygenase inhibitor without antioxidant properties, either ascorbate or GSH provided significant tocopherol regeneration. Kinetic studies showed that tocopherol regeneration after the addition of ascorbate was essentially completed by 1 min. By contrast, GSH addition caused a steady increase in tocopherol which peaked after 10 min of its addition. To determine whether this rapid regeneration is chemical or enzymic, regeneration was studied in the presence of chloroform and methanol. Comparison of various reductants in this denaturing condition for enzymes showed that ascorbate and NDGA afforded significant regeneration whereas GSH was ineffective, indicating that there are distinct enzymic and non-enzymic mechanisms for tocopherol regeneration. This study provides direct evidence from mass analysis that tocopherol can be regenerated in human cell homogenates. This finding implies that maintenance of membrane tocopherol status may be an essential function of ascorbate and GSH which operate in concert to ensure maximum membrane protection against oxidative damage.

Vitamin E and stress. I. Dietary unsaturated fatty acid stress and the metabolism of alpha-tocopherol in the rat.

1. A critical analysis of the biological antioxidant theory of vitamin E function has been made and the implications of the theory have been tested.2. When small amounts of [5-Me-14C]α-tocopherol were present in lipid systems subject to autoxidation in vitro, it was found that, whether the tocopherol was the sole antioxidant or was in synergistic combination with a secondary antioxidant (ascorbic acid), peroxidation did not occur without concomitant destruction of the tocopherol. This was so, whether a simple fat substrate or a liver homogenate (subject to catalysis) was used. The decomposition of tocopherol took place even when the secondary antioxidant was in large excess, as would occur under physiological conditions in the vitamin E-deficient animal, and accelerated as the induction period neared its end.3. When [5-Me-14C,3H]α-tocopherol and ascorbic acid were used as a synergistic antioxidant couple in vitro, tocopherol recovered from the peroxidizing system always had the same isotopic ratio as the starting material. This means that regeneration of tocopherol by the secondary antioxidant cannot involve, as an intermediate, a tocopherol carbon radical formed by loss of hydrogen from the 5-methyl group. Such radicals probably dimerize before they can be regenerated. The same result was found when doubly labelled α-tocopherol was given to the rat and recovered later from its tissues.4. In a series of experiments, rats were rigorously depleted of vitamin E for periods up to 7 months and then given as little as 50 μg [14C]D-α-tocopherol. They were then given, either by stomach tube daily or by dietary addition, large amounts of methyl linoleate or vitamin E-free polyunsaturated fatty acid methyl esters prepared from cod-liver oil and compared with controls given methyl oleate for up to 31 days. When the possibility of interaction between the lipid and tocopherol in the gut was eliminated, analyses of liver, kidney, testis, adrenal, adipose tissue, whole carcass and faeces showed that there was no effect of the polyunsaturated fatty acids on either the metabolism or recovery of [14C]α-tocopherol in any of the animals.5. When interaction between the administered fatty acid esters and tocopherol in the gut was allowed to take place, a marked destruction of [14C]α-tocopherol in the tissues was observed in animals given the polyunsaturated esters. The importance of oxidative destruction of tocopherol in the gut before absorption was demonstrated in a nutritional trial, in which cod-liver oil and lard were compared and the degrees of resistance of rats' erythrocytes to dialuric acid-induced haemolysis was used as an index of vitamin E depletion.6. Similar experiments with [14Cα-tocopherol in weanling rats given large amounts of cod-liver oil methyl esters also showed little effect. Although there was a suggestion that prolonged feeding of partly peroxidized polyunsaturated esters could lead to a slight depression of tissue tocopherol concentrations, no significant differences were usually obtained.7. Fourteen-day-old rats were given a vitamin E-deficient diet and received three weekly doses of 0.5 mg α-tocophcryl acetate. The dosage was stopped, the rats were then given a deficient diet containing 4% of either vitamin E-free linseed oil fatty acids or oleic acid, and the rate of their tocopherol depletion was measured by the erythrocyte haemolysis test. No effect of the polyunsaturated fatty acids was found. Nor was there any effect on the concentrations of ‘secondary antioxidants’ (glutathione and ascorbic acid) in liver, kidney, testis, muscle or adipose tissue.8. The results of the experiments in vivo contrast strongly with those in vitro. They lead to the conclusion that lipid peroxidation, if it occurs in the living animal, is irrelevant to the problem of vitamin E function. This conclusion has been substantiated by a critical review of the literature on the quantitative aspects of the vitamin E-dietary fat relationship.9. The effects of dietary fat stress in vitamin E-deficient animals are, we believe, due to two causes: (1) destruction of tocopherol in the diet or in the gastro-intestinal tract of the animal, and (2) the existence of an increased requirement for vitamin E for the metabolism of certain long-chain fatty acids. The specific effects of certain of these substances in producing or accelerating some vitamin E deficiency diseases may be related to the toxic states known to be induced in vitamin E-deficient animals by other stress factors.