Reaction Properties of the Ascorbic Acid Oxidase from Myrothecium verrucaria

Ascorbic acid oxidase activity in Myrothecium verrucaria extracts resulted in O(2) uptake exceeding 0.5 mole per mole of ascorbic acid and in CO(2) evolution. Measurement of oxidized ascorbic acid at completion of the reaction demonstrated that an average of 10% of the oxidized product disappeared. A comparison of the gas exchange data with the amount of ascorbic acid not accounted for indicated that the reaction could not be explained by independent oxidase and oxygenase systems. Chromatographic examination of the reaction mixtures identified l-threonic acid. Experiments with ascorbic acid-1-(14)C showed that C-1 was partially decarboxylated during the oxidation. Test of the fungal extracts for enzymes that might explain the deviation from expected stoichiometry showed that phenolase, glutathione reductase, cytochrome oxidase, peroxidase and oxalic decarboxylase were not involved. Addition of azide in concentrations sufficient to block catalase increased excess O(2) consumption about 65%. No enzymes were found that could directly attack oxidized ascorbic acid. H(2)O(2) accumulated during oxidation in azide-blocked systems.The O(2) excess could be explained by assuming the enzyme had peroxidative capacity on a reductant other than ascorbic acid. An intermediate of ascorbic acid oxidation appeared to function as the substrate yielding CO(2) and l-threonic acid on degradation. The increase in excess O(2) utilized in azide-blocked systems and the H(2)O(2) accumulation also were explained by the proposed scheme.Another interpretation would involve production of free radicals during ascorbic acid oxidation. Evidence for this was the ability of extracts to oxidize DPNH in the presence of ascorbic acid. Oxygen radicals formed in such reactions were considered possible agents of degradation of ascorbic acid.     

Ascorbic Acid in Neural Tissues

Abstract: Large amounts of ascorbic acid were readily removed from neural tissue by washing with warmed saline solutions. In areas where the original level was highest, such as cortex and cerebellum, a higher percentage was removed than from areas of lower concentration, such as pons-medulla. The residual level in both types of tissue was similar. During scurvy, the ascorbic acid retained in the guinea pig brain is more readily removed by washing than is that of the normal brain.     

抗坏血酸增强氯高铁血红素诱导的溶血

研究抗坏血酸对氯高铁血红素所诱导的红细胞溶血的影响.红细胞溶血采用在540 nm处测定 上清液血红蛋白吸光度的方法;红细胞巴比妥酸反应产物 (TBARS)测定采用Stocks 等建立的方法;高铁血红蛋白的测定采用Sezebeni等报道的方法.结果表明：抗坏血酸显著增强氯高铁血红素所诱导的溶血.尽管氯高铁血红素本身并不影响红细胞TBARS和高铁血红蛋白的水平,但是,氯高铁血红素和抗坏血酸一起诱导红细胞TBARS和高铁血红蛋白含量的增加;过氧化氢酶显著地抑制抗坏血酸增强氯高铁血红素诱导红细胞的溶血、TBARS和高铁血红蛋白的生成;氢氧自由基淬灭剂显著地抑制抗坏血酸增强氯高铁血红素诱导红细胞溶血.由上述可得到如下 结论：抗坏血酸增加氯高铁血红素诱导的红细胞氧化压力与H₂O₂有关;氢氧自由基可能是抗坏血酸增强氯高铁血红素诱导红细胞溶血的原因;抗坏血酸在氯高铁血红素存在时,可以作为一个亲氧化剂而非一个抗氧化剂.     

Urinary Hydroxyproline in the Elderly with Low Leucocyte Ascorbic Acid Levels

Fourteen elderly patients aged 58 to 91 with varying leucocyte ascorbic acid levels had urinary hydroxyproline/creatinine ratios measured before, during, and after treatment with ascorbic acid 1 g. daily for six days. The ratio increased during treatment in those patients whose initial ascorbic acid levels were below 15μg./10⁸ white blood cells. It is suggested that collagen metabolism may be impaired in these patients, and that all such patients should receive ascorbic acid supplements.     

Treatment of Irradiated Mice with High-Dose Ascorbic Acid Reduced Lethality

Ascorbic acid is an effective antioxidant and free radical scavenger. Therefore, it is expected that ascorbic acid should act as a radioprotectant. We investigated the effects of post-radiation treatment with ascorbic acid on mouse survival. Mice received whole body irradiation (WBI) followed by intraperitoneal administration of ascorbic acid. Administration of 3 g/kg of ascorbic acid immediately after exposure significantly increased mouse survival after WBI at 7 to 8 Gy. However, administration of less than 3 g/kg of ascorbic acid was ineffective, and 4 or more g/kg was harmful to the mice. Post-exposure treatment with 3 g/kg of ascorbic acid reduced radiation-induced apoptosis in bone marrow cells and restored hematopoietic function. Treatment with ascorbic acid (3 g/kg) up to 24 h (1, 6, 12, or 24 h) after WBI at 7.5 Gy effectively improved mouse survival; however, treatments beyond 36 h were ineffective. Two treatments with ascorbic acid (1.5 g/kg × 2, immediately and 24 h after radiation, 3 g/kg in total) also improved mouse survival after WBI at 7.5 Gy, accompanied with suppression of radiation-induced free radical metabolites. In conclusion, administration of high-dose ascorbic acid might reduce radiation lethality in mice even after exposure.     

Ascorbic Acid in Fetal Rat Brain

Ascorbic acid in fetal rat brain increases from 374 mg/g on the 15th day of gestation to 710 mg/g by the 20th day and remains at that level until birth. There is an 18% drop from this plateau after birth.