title: Dehydroascorbate influences the plant cell cycle through a glutathione-independent reduction mechanism.
abstract: Glutathione is generally accepted as the principal electron donor for dehydroascorbate (DHA) reduction. Moreover, both glutathione and DHA affect cell cycle progression in plant cells. But other mechanisms for DHA reduction have been proposed. To investigate the connection between DHA and glutathione, we have evaluated cellular ascorbate and glutathione concentrations and their redox status after addition of dehydroascorbate to medium of tobacco (Nicotiana tabacum) L. cv Bright Yellow-2 (BY-2) cells. Addition of 1 mm DHA did not change the endogenous glutathione concentration. Total glutathione depletion of BY-2 cells was achieved after 24-h incubation with 1 mm of the glutathione biosynthesis inhibitor l-buthionine sulfoximine. Even in these cells devoid of glutathione, complete uptake and internal reduction of 1 mm DHA was observed within 6 h, although the initial reduction rate was slower. Addition of DHA to a synchronized BY-2 culture, or depleting its glutathione content, had a synergistic effect on cell cycle progression. Moreover, increased intracellular glutathione concentrations did not prevent exogenous DHA from inducing a cell cycle shift. It is therefore concluded that, together with a glutathione-driven DHA reduction, a glutathione-independent pathway for DHA reduction exists in vivo, and that both compounds act independently in growth control.
authors.affiliation: Laboratory of Plant Physiology, Department of Biology, University of Antwerp, B-2020 Antwerp, Belgium. geert.potters@ua.ac.be
authors.forename: Geert
authors.initials: G
authors.lastname: Potters
authors.forename: Nele
authors.initials: N
authors.lastname: Horemans
authors.forename: Silvia
authors.initials: S
authors.lastname: Bellone
authors.forename: Roland J
authors.initials: RJ
authors.lastname: Caubergs
authors.forename: Paolo
authors.initials: P
authors.lastname: Trost
authors.forename: Yves
authors.initials: Y
authors.lastname: Guisez
authors.forename: Han
authors.initials: H
authors.lastname: Asard
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D002453:Cell Cycle / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D003683:Dehydroascorbic Acid / Q000378:metabolism* / Q000494:pharmacology; D005978:Glutathione / Q000378:metabolism*; D005980:Glutathione Reductase; D009247:NADH, NADPH Oxidoreductases / Q000037:antagonists & inhibitors / Q000378:metabolism; D009607:Nitrosourea Compounds / Q000494:pharmacology; D010084:Oxidation-Reduction / Q000187:drug effects; D010944:Plants / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D013880:Thioredoxin-Disulfide Reductase
chemical_list: D009607:Nitrosourea Compounds; D009247:NADH, NADPH Oxidoreductases; D005980:Glutathione Reductase; D013880:Thioredoxin-Disulfide Reductase; C424443:Txnrd3 protein, mouse; D005978:Glutathione; D003683:Dehydroascorbic Acid