Advertisement

Relationships Between Ascorbic Acid and Glutathione in Antioxidant Defense

  • A. F. Casini
  • E. Maellaro
  • B. Del Bello
  • L. Sugherini
  • M. Comporti
Part of the Developments in Oncology book series (DION, volume 71)

Abstract

A number of antioxidant systems protect cells against oxidative stress. Among these, ascorbic acid (AA) is generally believed to play an important role both in scavenging aqueous radicals and in regenerating vitamin E. The efficiency of AA as an antioxidant is readily apparent in in vitro systems in which isolated hepatocytes are incubated with prooxidants. We have shown, for instance, that high intracellular levels of AA afford a marked protection against allyl alcohol-induced lipid peroxidation and cell death, despite a quite similar glutathione (GSH) depletion (1). The antioxidant activity of AA results in AA consumption with formation of semidehydroascorbic acid radicals which, by dismutation, can produce dehydroascorbic acid (DHAA). The latter can be converted to degradation products, but can also bind to cellular macromolecules, thus producing toxic effects. Therefore, the cellular systems capable of reducing the oxidized forms of AA are important in eliminating such toxic effects and in restoring the antioxidant potential of AA. Evidence (2, 3) suggests that GSH is involved in the redox cycling of AA by rapidly reducing the oxidized forms of the latter. In fact the addition of DHAA to isolated hepatocytes results (1) in a marked increase of the intracellular content of AA at the expenses of GSH, which is oxidized to GSSG. Pretreatment of the hepatocytes with diethylmaleate or 1,3-bis(2-chloroethyl-1- nitrosourea) (BCNU) strongly decreases the capacity of the hepatocytes to reduce DHAA to AA.

Keywords

Ascorbic Acid Colon Mucosa Chemical Reduction Redox Cycling Dehydroascorbic Acid 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Casini, A.F., Maellaro, E., Del Bello, B., Sugherini, L. and Comporti, M. unpublished results.Google Scholar
  2. 2.
    Hughes, R.E. Nature 203: 1068–1069, 1964.PubMedCrossRefGoogle Scholar
  3. 3.
    Stahl, R.L., Liebes, L.F. and Silber, R. Biochim.Biophys.Acta 839:119–121, 1985.PubMedCrossRefGoogle Scholar
  4. 4.
    Choi, J.L. and Rose R.C. Proc.Soc.Exp.Biol.Med. 190: 369–374, 1989.PubMedGoogle Scholar
  5. 5.
    Wells, W.W., Peng Xu, n., Yang, Y. and Rocque, P.A. J.Biol.Chem. 265:15361–15364, 1990.PubMedGoogle Scholar
  6. 6.
    Gibson, D.D., Hawrylko, J. and McCay P.B. Lipids 20: 704–711, 1985.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1993

Authors and Affiliations

  • A. F. Casini
    • 1
  • E. Maellaro
    • 1
  • B. Del Bello
    • 1
  • L. Sugherini
    • 1
  • M. Comporti
    • 1
  1. 1.Istituto di Patologia GeneraleUniversita di SienaSienaItaly

Personalised recommendations