ascorbic-acid and propionic-acid

Diphenylhexatriene-labeled phosphatidylcholine and propionic acid have been established as selective fluorescence markers for the continuous determination of oxidation processes in the lipid and aqueous phases of unfractionated human serum. Oxidation of the respective fluorophores leads to a decrease in fluorescence intensity from which the time-dependent degradation of the marker molecule can be determined. The lag times preceding the propagation of oxidation are representative for the antioxidative capacity of the system, which may be influenced by exogenous factors, e.g., the antioxidants from the diet. Supplementation of human serum by quercetin, rutin, vitamin E, vitamin C, or total apple phenolics in vitro led to a decrease in oxidizability depending on the oxidation marker and the hydrophobicity of the antioxidant. Quercetin and vitamin E showed a higher in vitro capacity of protecting lipoproteins against oxidation. In contrast, rutin and vitamin C were more efficient as inhibitors in the aqueous phase. The same effect on serum was found after dietary consumption of apples. This result is in line with the known observation that intake of plant polyphenols leads to an increase in serum levels of hydrophilic antioxidants.

Topics: Antioxidants; Ascorbic Acid; Biomarkers; Dietary Supplements; Diphenylhexatriene; Electrophoresis, Agar Gel; Female; Flavonoids; Fluorescent Dyes; Humans; Lipids; Lipoproteins; Male; Malus; Oxidation-Reduction; Phenols; Phosphatidylcholines; Plasma; Polymers; Propionates; Quercetin; Rutin; Staining and Labeling; Vitamin E; Water

Propionic acidemia is an inherited neurometabolic disorder characterized by progressive neurological deterioration with psychomotor delay/mental retardation, convulsions and coma, and whose pathophysiology is poorly unknown. In the present study, we investigated the effect of chronic administration (from the 5th to the 28th days of life) of propionic acid (PA), the major metabolite accumulating in tissues of patients affected by propionic acidemia, on the cognitive performance of adult rats in the Morris water maze task. PA doses ranged from 1.44 to 1.92 micromol/g body weight as a function of animal age. Control rats were treated with saline in the same volumes. Chronic postnatal days (5-28) PA treatment had no effect on body weight. However, it impaired spatial performance in the water maze. We also determined the effect of ascorbic acid (AA) administered, alone or combined with PA, on the same behavioral parameters in order to test whether free radicals could be responsible for the behavioral alterations observed in PA-treated animals. AA was able to prevent the behavioral alterations provoked by PA, implying that oxidative stress may be involved in these effects. Furthermore, we also investigated the total radical-trapping antioxidant potential (TRAP) in the hippocampus of the animals. We observed that TRAP was significantly reduced in the brain of propionic acidemic rats and that co-administration of AA prevented this effect. The results provide evidence that early PA treatment induces long-lasting behavioral deficits, which are possibly caused by oxygen reactive species generation, and suggest that oxidative stress may be involved in the neuropathology of propionic acidemia.

Topics: Animals; Ascorbic Acid; Body Weight; Cognition Disorders; Free Radical Scavengers; Hippocampus; Male; Maze Learning; Propionates; Rats; Rats, Wistar; Reactive Oxygen Species; Reversal Learning; Swimming

Illumination by visible light (400 Ix) of cultures containing larvae of Drosophila melanogaster can reduce survival (Bruins et al., Insect Biochemistry 21:535-539, 1991). Here we show that the effect of light depends on the presence of propionic or acetic acid in the food medium. We also show that survival is far more affected by illumination of the yeast food media than by direct illumination of the eggs and developing larvae. It is shown that addition of antioxidants to the food prevents light induced mortality. The action of antioxidants suggests that free radicals are important in light induced mortality. We also showed that both yeast and riboflavin (vitamin B2) solutions illuminated with visible light (400 Ix) generate hydrogen peroxide. Other vitamin and amino acid solutions do not produce peroxide in measurable amounts. However, the concentration of photogenerated hydrogen peroxide is far too low to explain the death of eggs and developing larvae upon exposure to light. A 400 Ix light treatment destroys the capability of yeast food media to support survival of larvae. Addition of vitamin C, carotene, tryptophan, nipagin, uric acid, or sucrose to the light treated medium does not restore viability. It is restored when riboflavin is added to the photo-inactivated yeast. A high concentration of pyridoxine also produced an improvement in survival. When riboflavin is treated with light, it cannot support survival on synthetic food media nor can it restore survival on light treated yeast food media. These results show that riboflavin (or a derivative) is a major light sensitive compound of yeast, which can be degraded by light. Light induced loss of riboflavin leads to mortality, because this is an essential dietary vitamin. The vitamin degradation can be prevented by dietary antioxidants. A chromatographic analysis confirms this conclusion.

Topics: Acetic Acid; Animals; Antioxidants; Ascorbic Acid; Culture Media; Drosophila melanogaster; Hydrogen Peroxide; Larva; Propionates; Riboflavin; Saccharomyces cerevisiae; Vitamins

Four Staphylococcus aureus strains were incubated at 37 degrees C for 24 h in broth progressively acidified with lactic, citric, ascorbic, acetic, pyruvic and propionic acids, and their survival rate and enterotoxin producing ability was studied. Acids were chosen based on their frequent use by the food industry. Periodically, samples were withdrawn to determine counts, pH and the presence of enterotoxins A, B, C, and D. For a given acid, the effect on growth and enterotoxin synthesis was different. The most inhibitory acid for the growth of strains FRI-100 and FRI-472 was pyruvic acid, for strain FRI-137 was lactic acid, all six acids were equally effective on strain S6. Lactic acid was very inhibitory to enterotoxin synthesis, but the effect on this parameter of acetic and citric acids was almost nil. Enterotoxins were seen to be inactivated at acid pH values; enterotoxin B was the most resistant to inactivation.

Topics: Acetates; Acetic Acid; Ascorbic Acid; Carboxylic Acids; Citrates; Citric Acid; Enterotoxins; Enzyme-Linked Immunosorbent Assay; Food Microbiology; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Propionates; Pyruvates; Pyruvic Acid; Staphylococcus aureus