ABSTRACT
Maize (Zea mays L. cv kanaujia) plants grown with Zn [10 (control), 0.1 (low) and 20 microM (high)], were investigated for concentration of antioxidants and activities of antioxidative enzymes in leaves. Young leaves of low Zn plants developed whitish-necrotic spots. Leaves of both low and high Zn plants showed decrease in chlorophyll concentration and accumulation of lipid peroxides, ascorbate and dehydroascorbate, associated with a decrease in the activity of ascorbate peroxidase and superoxide dismutase. Low and high Zn, however, showed diverse effect on glutathione reductase. While low Zn increased the activity of glutathione reductase, high Zn decreased its activity. Zinc effect on antioxidative constituents suggested Zn involvement in sustaining the antioxidative defense system in maize leaves.
Subject(s)
Antioxidants/metabolism , Ascorbic Acid/metabolism , Chlorophyll/metabolism , Dehydroascorbic Acid/metabolism , Glutathione Reductase/metabolism , Lipid Peroxides/metabolism , Necrosis , Peroxidases/metabolism , Plant Leaves/enzymology , Superoxide Dismutase/metabolism , Zea mays/drug effects , Zinc/pharmacologyABSTRACT
Pro-oxidant properties of ascorbate have been studied with uses of brain tissues and neuronal cells. Here we address potential mechanism of ascorbate coupling with glutamate to generate oxidative stress, and the role which oxidized ascorbate (dehydroascorbate) transport plays in oxidative neuronal injury. Ascorbate in neurones can be depleted by adding glutamate in culture medium since endogenous ascorbate can be exchanged with glutamate, which enhances ascorbate/ dehydroascorbate transport by depleting ascorbate in the neurons with the glutamate-heteroexchange. However, ascorbate is known readily being oxidized to dehydroascorbate in the medium. Glutamate enhanced the dehydroascorbate uptake by cells via a glucose transporter (GLUT) from extracellular region, and cytosolic dehydroascorbate enhanced lipid peroxide production and reduced glutathione (GSH) concentrations. Iso-ascorbate, the epimer of ascorbate was ineffective in generating the oxidative stress. These observations support the current concept that the high rates of dehydroascorbate transport via a GLUT after the release of ascorbate by glutamate leads to peroxidation, the role of glutamate on ascorbate/ dehydroascorbate recycling being critical to induce neuronal death via an oxidative stress in the brain injury.
Subject(s)
Animals , Male , Rats , Ascorbic Acid/analogs & derivatives , Biological Transport/drug effects , Cerebral Cortex/drug effects , Cytochalasin B/pharmacology , Dehydroascorbic Acid/metabolism , Glutamic Acid/pharmacology , Glutathione/metabolism , In Vitro Techniques , Lipid Peroxidation/drug effects , Oxidation-Reduction/drug effects , Oxidative Stress/drug effects , Rats, Sprague-Dawley , Thiobarbituric Acid Reactive Substances/metabolismSubject(s)
Adolescent , Ascorbic Acid/metabolism , Dehydroascorbic Acid/metabolism , Female , Humans , Leukemia, Myeloid/blood , Leukocytes/metabolism , Male , Middle AgedABSTRACT
Dehydroascorbic acid is present in insignificant amounts in plant and animal tissue but appears in considerable amounts under various physiological and pathological conditions. It is found increased: in blood of patients suffering from infectious diseases; in blood and tissues of thyrotoxic patients; in blood after injection of thyroxin, corticotropin and cortisone. In all the above conditions there is concomitant decrease in L-ascorbic acid and glutathione values of blood and tissues. Dehydroascorbic acid, however, disappears after continued administration of a high dose of ascorbic acid. The accumulation of dehydroascorbic acid seems to be an indication of ascorbic acid deficiency. The extreme sensitivity of the ascorbate system to physiological changes is suggestive of a major biochemical role for this redox system. Accumulated evidences indicate that dehydroascorbic acid possible control cell division.