Iron (II) Ions Induced Oxidation of Ascorbic Acid and Glucose

Abstract

Lipid peroxidation (LPO) of polyunsaturated fatty acids (PUFAs) is suspected to be involved in the generation of chronic diseases. A model reaction for LPO is the air oxidation of PUFAs initiated by Fe2+ and ascorbic acid. In the course of such model reactions glycolaldehyde (GLA) was detected as main aldehydic product. Since it is difficult to explain the generat on of GLA by oxidation of PUFAs, it was suspected that GLA might be derived by oxidation of ascorbic acid. This assumption was verified by treatment of ascorbic acid with Fe2+. Produced aldehydic compounds were trapped by addition of pentafluorobenzylhydroxylamine hydrochloride (PFBHA-HCl), trimethylsilylated and finally identified by gas chromatography/mass spectronetry (GC/MS). Oxidation of ascorbic acid with O2 in presence of iron ions produced not only glycolaldehyde (GLA), but also glyceraldehyde (GA), dihydroxyacetone (DA) and formaldehyde. Glyoxal (GO) and malondialdehyde (MDA) were detected as trace compounds. The yield of the aldehydic compounds was increased by addition of lipid hydroperoxides (LOOH) or H2O2. The buffer influenced the reaction considerably: Iron ions react with Tris buffer by producing dihydroxyacetone (DA). Since ascorbic acid is present in biological systems and Fe2+ ions are obviously generated by cell damaging processes, the production of GLA and other aldehydic components might add to the damaging effects of LPO. Glucose suffers also oxidation to short-chain aldehydic compounds in aqueous solution, but this reaction requires addition of equimolar amounts of Fe2+ together with equimolar amounts of H2O2 or 13-hydroperoxy -9-cis-11-trans-octadecadienoic acid (13-HPODE). Therefore this reaction, also influenced by the buffer system, seems to be not of biological relevance.

Buffer interactions: Densities and solubilities of some selected biological buffers in water and in aqueous 1,4-dioxane solutions

“…To fulfill its function, an ideal biological buffer should not only possess the correct pK a and buffer capacity but should also produce no adverse effects on biochemical reactions [1][2][3], and there may be no one ideal buffer for a given pH range. For example, TRIS [1], HEPES, and Tricine buffers have been shown to react with radicals [4][5][6][7], and TRIS has also been shown to react with aldehydes [8][9][10][11][12]. It is important to carry out measurements in more than one kind of buffer to establish which buffers cause least disturbance to the system under study, the usual criterion being that the observed reaction rates or transformations are maximal.…”

Transcriptional Activation of the Aldehyde Reductase YqhD by YqhC and Its Implication in Glyoxal Metabolism of Escherichia coli K-12

“…Glyoxal (GO) is a reactive ␣-oxoaldehyde formed by the oxidative degradation of glucose, by lipid peroxidation, and by the autoxidation of ascorbic acid (21,38). Due to its two reactive carbonyl groups, GO is capable of inducing cellular damage through multiple mechanisms.…”

Novel Monoclonal Antibody Recognition of Oxidative DNA Damage Adduct, Deoxycytidine-Glyoxal

“…3). It has been demonstrated previously that this reaction system readily induces glyoxalation of DNA (Mistry et al, 1999), where glyoxal is generated as a product of oxidative ascorbate degradation (Mlakar et al, 1996). The dose-dependent binding observed between ascorbate-modified DNA and Ab F3/9 was significantly reduced in the presence of catalase (500…”

“…Glyoxal, a dialdehyde product of the autoxidation of lipids (Loidl-Stahlhofen and Spiteller, 1994), ascorbic acid (Mlakar et al, 1996), and glucose (Kasai and Nishimura, 1986;Thornalley, 1985;Wells-Knecht et al, 1995), is also generated from the oxidative degradation of deoxyribose (Awada and Dedon, 2001;Mistry et al, 1999;Murata-Kamiya et al, 1995). It is suggested that glyoxal, generated from hydroxyl radical attack at C-4 or C-3 of deoxyribose, would readily modify nearby DNA bases.…”