Oxidation antioxidants, ascorbic acid

In its biochemical functions, ascorbic acid acts as a regulator in tissue respiration and tends to serve as an antioxidant in vitro by reducing oxidizing chemicals. The effectiveness of ascorbic acid as an antioxidant when added to various processed food products, such as meats, is described in entry on Antioxidants. In plant tissues, the related glutathione system of oxidation and reduction is fairly widely distributed and there is evidence that election transfer reactions involving ascorbic acid are characteristic of animal systems. Peroxidase systems also may involve reactions with ascorbic acid In plants, either of two copper-protein enzymes are commonly involved in the oxidation of ascorbic acid. 

Protection was not associated with MAO-B inhibition in that pargyline, a potent MAO inhibitor, was ineffective and pretreatment with pargyline did not prevent the protective effects of selegiline. Protection was not associated with inhibition of dopamine uptake by selegiline because the dopamine uptake inhibitor mazindol did not diminish BSO toxicity. Antioxidant ascorbic acid (200 iM) also protected BSO-induced cell death, suggesting that oxidative events were involved. This... 

Partial silylation of the highly disperse silica surface enhances the adsorption of vitamin E from ethanol solution, and provides the ability to obtain water-soluble nanocomposites containing vitamin E. Immobilization of vitamin C on the silica surface prevents its oxidation. Its interaction with the adsorbent surface leads to a decrease in proton-donor ability of the OH-groups involved in the oxidation of ascorbic acid. Elydrophobized silica nanocomposites are characterized by a prolonged desorption of immobilized vitamins. It has been shown that vitamin C does not lose its antioxidant properties after desorption. 

Studies on the antioxidant properties of anthocyanins on human low-density lipoprotein (LDL) and lecithin liposome systems in vitro showed that the inhibition of oxidation increased dose-dependently with antioxidant concentration. The oxidation was catalyzed by copper in the LDL system and the effects of the anthocyanins were explained by several antioxidant mechanisms including hydrogen donation, metal chelation and protein binding [33]. Anthocyanins also prevented the oxidation of ascorbic acid (vitamin C), through chelate formation with the metal ions, and finally by the formation of an ascorbic (copigment)-metal-anthocyanin complex [49]. 

Antioxidant Agent that inhibits oxidation and thus is used to prevent deterioration of preparations by oxidative process Ascorbic acid, ascorbyl palmitate, butylated hydroxyanisole, butylated hydroxytoluene, hypophosphorus acid, monothioglycerol, propyl gallate, sodium ascorbate, sodium bisulfite, sodium formaldehyde, sulfoxylate, sodium metabisulfite... 

The antioxidants studied can be classified into two broad types phenolic antioxidants and non-phenolic antioxidants. Phenolic antioxidants have been found to be more promising as they are obtained from dietary sources.Vitamin E (a-tocopherol), the first known chainbreaking antioxidant, is also an o-methoxy phenol. Pulse radiolysis studies of vitamin E and its water-soluble analogue, trolox C, have been reported several years ago. a-tocopherol reacts with almost all the oxidizing free radicals, and the phenoxyl radicals produced during oxidation reactions absorb at -460 nm (Fig. 1). The regeneration reaction of a-tocopherol phenoxyl radicals back to a-tocopherol by water-soluble antioxidant ascorbic acid was also first reported by pulse radiolysis method. The one-electron reduction potential of vitamin E is -0.48 V vs. NHE. Both a-tocopherol and trolox C are used as standards for evaluating the antioxidant ability of new compounds. 

Oxidation protection Antioxidants Ascorbic acid, glutathione, propyl gallate, vitamin E... 

The scientific community has been discussing for quite some time now the relationship between oxidative stress, defined as the imbalance between oxidant and antioxidants [45], and the health-disease status. An impressive amount of information available in the literature deals with the effects of the classic antioxidants, ascorbic acid, a-tocopherol, and jS-carotene in a huge series of pathophysiological situations in experimental animals and humans. Concerning the effects of the classic antioxidants on mitochondrial function in situations of oxidative stress, the information is not so vast and most of the time it is not conclusive. However, substantial progress has been made in the description of the mitochondrial alterations in neurodegenerative diseases and in the a-tocopherol effects,both as prevention and as treatment [46]. We will briefly review some reports related to vitamin E and mitochondrial dysfunction in oxidative metaboHc disorders and in the neurodegenerative Alzheimer s and Parkinson s diseases. 

To prevent oxidation of reduced organosulfur in the wood cell walls, conservators are currently investigating antioxidants. Commercial antioxidants (ascorbic acid, anthocyanidins, proanthocyanins, flavon-3-ols, flavonones and flavonols) are being used to prevent oxidation of reduced species by mopping up free radicals. 

The ready oxidation of ascorbic acid will catalyze chemical changes in a number of other substances. Thus, unsaturated fatty acids in lecithins and tissues are catalytically oxidized in the presence of ascorbic acid to a substance producing color with thiobarbiturate (B21). The product of the ascorbic acid-catalyzed oxidation is malonaldehyde, which can also inhibit L-gulonolactone oxidase, the enzyme forming ascorbic acid (Cl). It has been suggested that this enzyme inhibition may occur in vivo in animals deficient in vitamin E, a compound believed to have antioxidant actions which would prevent the ascorbic acid-catalyzed lipid oxidation from giving rise to malonaldehyde. It is quite probable that the active intermediate in the formation of malonaldehyde is the monodehydroascorbate radical which initiates the lipid oxidation. 

Under certain conditions ascorbic acid is an antioxidant probably because it readily loses H to abstraction. Attention also has been given to the prooxidative effect of ascorbic acid in the presence of transition metal ions (44). It is thought that ascorbic acid reduces metal ions which in turn are more effective in catalyzing lipid oxidation. Consequently, ascorbic acid becomes oxidized to dehydroascorbic acid. 

The quinone intermediate itself was not observed by this method, but may be the active species in the biological assay. The hydroxyquinone S6,721-l was stable in the presence of the antioxidant ascorbic acid or when helium was continuously supplied to the medium, confirming that the degradation is due to an oxidation step. 

Thiol depletion by culturing normal human foetal lung fibroblasts in cystine-free medium or with thiol-depleting agents induced oxidant accumulation and cell death by apoptosis (Aoshiba et al. 1999). The cell death was prevented by the antioxidants ascorbic acid and catalase. 

Destruction of vitamins A, C, D and E induced by riboflavin-photosensitized oxidation has been reported. Vitamin A and its esters, along with carotenoids with pro-vitamin A activity, undergo ring opening upon sunlight exposure in the presence of riboflavin. Although an excellent antioxidant, ascorbic acid is rapidly photooxidized in the presence of riboflavin. Even a small decrease in riboflavin content in milk due to photosensitization can lead to virtual complete destruction of ascorbic acid. Fortunately, milk is not an important source of vitamin C in most diets. 

Vitamin C is transported into the blood cells in its oxidized form as dehydroascorbic acid, since this form is non-ionized under physiological conditions and is therefore permeable for membranes. It has been postulated that at least human neutrophils are able to oxidize extracellular ascorbic acid for a more efficient uptake into the cells (Washko et al., 1993). This mechanism also represents a part of the biological recycling system for antioxidants. The intracellular dehydroascorbic acid is rapidly reduced again to ascorbic acid by the GSH redox system. This reduction might also be mediated by the still hypothetical dehydroascorbic acid reductase. 

Traces of heavy metal ions can act as catalysts for fat or oil oxidation. Their binding by chelating agents increases antioxidant efficiency and inhibits oxidation of ascorbic acid and fat-soluble vitamins. The stability of the aroma and color of canned vegetables is substantially improved. 

Food sample pretreatment may consist of either (a) saponification to quantify the free forms (retinol or xanthophylls may occur free or ester-ified in foods) [95,96] or (b) direct extraction to determine the unaltered A vitamers [84,88]. Alkaline hydrolysis is also an expedient to simplify the vitamin A analysis, since retinol is the only form to be quantified nevertheless, due to its sensitivity to light and oxygen, it is important to prevent photo-oxidation by inclusion of a antioxidant (ascorbic acid, hydroquinone, or pyrogallol). A drawback of hot saponification is the generation of artifacts, such as geometric isomers of retinol and carotenoids [97]. 

Other Acids. Ascorbic acid (3) is used primarily as an antioxidant and to a lesser extent as an added nutrient ia beverages. It oxidizes readily, preventing the oxidation of certain flavoting compounds. Tartaric (4) and adipic acids are used to a lesser extent ia grape flavored beverages. Malic acid can be used as an alternative to citric acid ia some fmit flavored beverages. 

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