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PubMed1989

Oxidation of Neurospora crassa NADP-specific glutamate dehydrogenase by activated oxygen species.

The glutamine synthetase and the NADP-specific glutamate dehydrogenase activities of Neurospora crassa were lost in a culture without carbon source only when in the presence of air. Glutamine synthetase was previously reported to be liable to in vitro and in vivo inactivation by activated oxygen species. Here we report that NADP-specific glutamate dehydrogenase was remarkably stable in the presence of activated oxygen species but was rendered susceptible to oxidative inactivation when chelated iron was bound to the enzyme and either ascorbate or H2O2 reacted on the bound iron. This reaction gave rise to further modifications of the enzyme monomers by activated oxygen species, to partial dissociation of the oligomeric structure, and to precipitation and fragmentation of the enzyme. The in vitro oxidation reaction was affected by pH, temperature, and binding to the enzyme of NADPH. Heterogeneity in total charge was observed in the purified and immunoprecipitated enzymes, and the relative amounts of enzyme monomers with different isoelectric points changes with time of the oxidizing reaction.

Aerobiosis↗
PubMed1992

An investigation of the relationship between free radical activity and vitamin C metabolism in elderly diabetic subjects with retinopathy.

Abnormalities of both free radical activity and ascorbic acid metabolism have been documented in diabetes, but their biological basis is unclear and their relationship unstudied in any detail. This study was designed to compare changes in antioxidant status and free radical reactions in a group of elderly diabetic patients (with and without retinopathy) with those in a group of age-matched control subjects. No significant differences in thiobarbituric acid (TBA) reactivity, red cell glutathione (GSH) concentrations or diene conjugates (DC) between patients and controls were seen despite significant depletion of ascorbic acid in patients with diabetes, especially in those with retinopathy. The results emphasise the present-day difficulties of measuring free radical activity and demonstrate a marked abnormality in ascorbic acid metabolism in diabetes.

Aged↗
PubMed2000

Interconversion between dehydro-L-ascorbic acid and L-ascorbic acid.

L-Ascorbic acid (AA) plays an important role in biological systems as an electron donor. Erythorbic acid (EA) is the epimer of AA and has chemical characteristics very similar to those of AA. It is demonstrated in the present study by 1H-NMR that dehydro-L-ascorbic acid (DAA) was reduced by EA under neutral conditions but not acidic, and that dehydroerythorbic acid (DEA) was also reduced by AA under the same conditions. These reactions also occurred at a low concentration close to the concentration of AA in such biological tissue as the liver. Furthermore, the interconversion of DAA and AA at neutral pH and low concentration was also confirmed by radioluminography. These results suggest the interconversion between DAA and AA in vivo.

Ascorbic Acid↗
PubMed2004

Vitamin C: basic metabolism and its function as an index of oxidative stress.

Vitamin C (ASC) is well known as an outstanding antioxidant in animal tissues. This concept is reviewed from a chemical standpoint, starting from a chemical view of radical reactions in the cell. ASC, vitamin E, and lipid hydroperoxide were selected as key molecules involved in radical reactions in the cell, and their efficiencies as an index of oxidative stress were evaluated. At first, methods for specific and sensitive determination of ASC and lipid hydroperoxide were developed. Based on comparisons of these indices during oxidative stress in typical pathological conditions, such as diabetes and liver damage by toxicants, ASC concentration was found to be the most sensitive index in animal tissues. Antioxidative effect of food factors in vivo can be evaluated on the basis of these indices. Analysis of oxidation of low-density lipoprotein (LDL) revealed that degradation and cross-link of apolipoprotein B-100 (apoB) are extremely facile processes. Fragmented and conjugated apoB proteins are present in normal human serum, and tend to increase with age based on immunoblot analysis. Estimation of these products allows us a mechanism-based diagnosis of atherosclerosis. A significant relationship between plasma ASC level and the sum of these apoB products was found. In conclusion, specifically determined ASC concentration sensitively reflects oxidative stress in tissues.

Animals↗
PubMed1986

Effects of lipophilic derivatives of L-ascorbic acid and dehydro-L-ascorbic acid on the peroxidation of linoleic acid in neutral phosphate buffer containing alcohol.

6-O-Palmitoyl-AsA (AP) and -DHA (DHAP) suppressed LA peroxidation considerably in both 10% and 20% EtOH solutions. The duration of the suppression of LA peroxidation was longer with AP than with DHAP. But after the initial suppression of LA peroxidation, both derivatives showed an accelerating effect. 6-O-Acetyl-AsA (Ac-AsA) and -DHA (Ac-DHA) accelerated LA peroxidation from the start of the reaction in 10% EtOH, but suppressed it notably in 20% EtOH. 4-Phenyl-2,3-dihydroxy-2-buten-4-olide (PDHB) and 4-phenyl-2,3-dioxo-4-butenolide (PDOB) accelerated LA peroxidation in 10% EtOH. With 20% EtOH solution, PDHB suppressed LA peroxidation notably, as did AP, but PDOB showed only a short duration (about 1 h) of suppression. These results suggest the complexity of LA peroxidation catalyzed by lipophilic AsA or DHA in aqueous solution containing alcohol.

4-Butyrolactone↗
PubMedDate not supplied

[Ascorbic acid radicals induced by the action of radiation in tissues from rat organs frozen at 77 K].

Subsequent annealing technique and computer assistant analysis of EPR spectra were used to isolate an asymmetric EPR signal Rs(g = 2,0051; delta H = 0.8 mT) from the EPR spectrum of rat spleen gamma-irradiated at 77 K. Radicals with the same EPR spectrum were registered in: 1) water solution of ascorbic acid (2.10(-2) M, pH 3.4) frozen and irradiated at 77 K and 2) water-glycerol solution of ascorbic acid (10(-2) M, pH 10.3) frozen rapidly at the moment of intensive autooxidation. These model experiments allow to conclude that Rs signal is caused by the radicals of semidehydroascorbic acid. Radiochemical yield of these radicals as well as of all the radicals induced by gamma radiation in the whole rat tissues were measured. The EPR signal (Rs) is equivalent to the well known "artifact" signal of lyophilized tissues. The explanation of the mechanism of the radicals formation taking place under annealing of the frozen and irradiated tissues was suggested.

Animals↗
PubMed1983

Modulation of alkaline phosphatase in different organs by ascorbic acid and related compounds.

The organ-specific modulation by ascorbic acid and related compounds on alkaline phosphatase activity of calf intestinal and human placental tissues has been studied at pH 8.0 and 37 degrees C. L(+)-ascorbic acid and its isomer D(-)-ascorbic acid inhibit to a similar extent the intestinal isoenzyme and appear to be more potent modifiers than dehydro-L-(+)-ascorbic acid. In contrast, the placental isoenzyme shows an initial activation by the three chemical agents, followed by an inhibition. The inhibition is lower with L(+)-ascorbic acid and D(-)-ascorbic acid, while its catalytic activity is affected only slightly by dehydro-L-(+)ascorbic acid.

Alkaline Phosphatase↗
PubMed1994

Recovery of antioxidants and reduction in lipid hydroperoxides in murine epidermis and dermis after acute ultraviolet radiation exposure.

In previous studies we have found that a single acute dose of ultraviolet radiation to murine skin causes a large degree of destruction of enzymic and non-enzymic antioxidants immediately after irradiation. In the present study, we wished to elucidate the recovery of antioxidants after a single dose of ultraviolet (UV) radiation. We measured antioxidants and lipid hydroperoxides (as a marker of membrane damage) in murine epidermis and the dermis at 0, 3, 12, 24, 72 and 120 h after exposure to UV radiation (25 J/cm2, UVA+UVB). Lipid hydroperoxides showed the highest values immediately after UV exposure and returned to control values within 24 h in both epidermis and dermis. The activities of catalase, glutathione peroxidase and glutathione reductase showed the lowest activities immediately after UV exposure; superoxide dismutase activities reached a minimum at 3 h postexposure. The pattern of recovery was different for each enzyme and for epidermis and dermis. The activities of superoxide dismutase and catalase decreased remarkably and recovered slowly. Superoxide dismutase in the dermis recovered full activity by 120 h and in the epidermis by 12 h. Catalase activity in both epidermis and dermis had returned to only 50% of control activity at 120 h, although the epidermis showed a temporary increase (to 93%) at 24 h. Glutathione peroxidase and glutathione reductase were slightly decreased immediately after irradiation, recovered to 100% at 3 h and then increased to 200-250% in both the epidermis and the dermis at various times; values had returned to 100% in epidermis by 120 h but remained elevated in dermis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Ascorbic acid oxidation product(s) protect human low density lipoprotein against atherogenic modification. Anti- rather than prooxidant activity of vitamin C in the presence of transition metal ions.

The oxidative modification of low density lipoprotein (LDL) has been proposed as an important causative event in the development of human atherosclerosis. As a corollary of this hypothesis, antioxidants that can prevent LDL oxidation may inhibit atherosclerosis. Oxidative modification of LDL in vitro, either induced by Cu2+ or mediated by cultured arterial wall cells in media containing trace amounts of transition metal ions, is strongly inhibited by vitamin C (L-ascorbic acid (AA)). AA, however, is known to act as a prooxidant rather than an antioxidant in the presence of transition metal ions. We observed that AA is oxidized rapidly when incubated with Cu2+ and LDL, leading to transient formation of dehydro-L-ascorbic acid (DHA). Although AA and DHA can no longer be detected after 3.5 h of incubation, LDL resists oxidative modification for at least 20 h, as assessed by anodic gel electrophoretic mobility. Remarkably, DHA protects LDL more effectively against both Cu(2+)-induced lipid peroxidation and shifts in electrophoretic mobility than does AA; indeed, AA per se, without oxidation to DHA, offers no protection. By inhibiting oxidative modification of LDL, AA and DHA prevent uptake of LDL by macrophages via the scavenger receptor pathway. When LDL is incubated with DHA followed by gel filtration, LDL remains protected against subsequent Cu(2+)-induced oxidative modification, suggestive of stable modification of LDL in the presence of DHA. In contrast, DHA is ineffective against a metal ion-independent type of oxidative stress, viz. aqueous peroxyl radicals; under these conditions, only AA is able to inhibit lipid peroxidation in LDL. Our data indicate that vitamin C protects LDL against atherogenic modification by two different mechanisms that may act in concert: (i) free radical scavenging by AA prevents aqueous oxidants from attacking and oxidizing LDL, and (ii) stable modification of LDL by DHA or decomposition product(s) thereof imparts increased resistance to metal ion-dependent oxidation.

Adult↗
PubMed1975

[Metabolism of L-ascorbic, L-dehydroascorbic and 2,3-diketo-L-gulonic acids during a short duration fast in guinea pigs].

Tricolor variety of guinea-pigs, two or three months old, received, without sex distinction L(+)-ascorbic or L(+)-dehydroascorbic acids intraperitoneally injections as 20 mg p. 100 by weight, three or twenty-four hours after starting a forty-eight hours fast. Ascorbic, dehydroascorbic and 2,3 diceto-L-gulonic acids are estimated by the Roe, Mills, Oesterling and Damron differential 2,4-dinitrophenylhydrazin method in whole blood, urines, kidneys and liver. Food absorption during twenty-four hours after the end of the forty-eight hours fast is not suffisant for guinea-pigs regain first state, during this time, especially in their kidneys and liver. Three hours after the beginning of the fast, urinary excretion of the injected acid increases during the first twenty-four hours of fast; at the end of the forty-eight hours fast their kidneys are deficient in ascorbic acid. Twenty-four hours after the beginning of fast, urinary excretion of ascorbic, dehydroascorbic and 2,3-diceto-L-gulonic acids rises importantly, especially when L-ascorbic acid is injected; it is only the quantity of ascorbic acid which increases in their kidneys and liver, its level being higher in their liver. L-dehydroascorbic acid is utilized immediately. L-ascorbic acid is distributed slowly, stored in a reduced form and it prepares the animals to face a prolonged fast. When the animals are injected three hours after the fast begins, it will be protected for forty-eight hours; if it is injected twenty-four hours after the beginning of fast, the animal will be better prepared to face a prolonged state of stress or a fast lasting more than forty-eight hours.

2,3-Diketogulonic Acid↗
PubMed1983

Studies on the metabolic conversion of ascorbate.

In the intact animal guinea pigs metabolize (1-14C)ascorbic acid much faster to (14C)carbon dioxide (peak exhalation at 30 min) than rats (peak exhalation at 2 to 3 h) following single oral administration, but total excretion was comparable. This finding might be related to the differences in the absorption mechanism of ascorbic acid in these species. The large difference in retention capacity of ascorbic acid in the liver is suggested to be due to multiple recirculation of ascorbic acid in the guinea pig when compared to the rate. Homogenate preparations of rat stomach, small intestine or liver as well as cultured intestinal microbial flora did not cause metabolic degradation on incubation with (1-14C)ascorbic acid to (14C)carbon dioxide. It is therefore suggested that the observed excretion of (14C)carbon dioxide is due to spontaneous non-enzymatical reaction in liver and possible other tissues. Analysis of ascorbic acid metabolites formed on incubation by analytical isotachophoresis suggests that ascorbic acid is a rather stable substrate whereas dehydroascorbate and 2,3-diketogulonic acid are rapidly degraded. This allows the assumption that in vivo metabolism of ascorbic acid might not involve dehydroascorbic acid. Our data do not support the hypothesis that ascorbic acid undergoes presystemic metabolism to carbon dioxide in the intestinal wall.

2,3-Diketogulonic Acid↗