Role of vitamin E in ascorbate-dependent protein thiol oxidation in rat liver endoplasmic reticulum.

Abstract

Addition of ascorbate or its generation from gulonolactone causes the oxidation of protein thiols and a simultaneous dehydroascorbate formation in rat liver microsomes. The participation of vitamin E in the phenomenon was studied. We measured ascorbate and protein thiol oxidation and lipid peroxidation in vitamin E deficient liver microsomes. Vitamin E deficiency partly uncoupled the two processes: ascorbate oxidation increased, while protein thiol oxidation decreased. These changes were accompanied with an accelerated lipid peroxidation in the vitamin E-deficient microsomes, which indicates the accumulation of reactive oxygen species. All these effects were reduced by the in vitro addition of vitamin E to the deficient microsomes, supporting its direct role in the process. The results demonstrate that vitamin E is a component of the protein thiol oxidizing machinery in the hepatic endoplasmic reticulum transferring electrons from the thiol groups towards oxygen.

• Authors: M Csala, A Szarka, E Margittai, V Mile, T Kardon, L Braun, J Mandl, G Bánhegyi
• Journal: Archives of biochemistry and biophysics (Arch Biochem Biophys) Vol. 388 Issue 1 Pg. 55-9 (Apr 01 2001) ISSN: 0003-9861 [Print] United States
• PMID: 11361140 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Reactive Oxygen Species
• Sulfhydryl Compounds
• Vitamin E
• Ascorbic Acid

Topics

• Animals
• Ascorbic Acid (metabolism)
• Electrons
• Endoplasmic Reticulum (metabolism)
• Liver (metabolism)
• Male
• Microsomes, Liver (metabolism)
• Models, Biological
• Rats
• Rats, Wistar
• Reactive Oxygen Species
• Sulfhydryl Compounds (metabolism)
• Time Factors
• Vitamin E (physiology)
• Vitamin E Deficiency (metabolism)