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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. Role of vitamin E in ascorbate-dependent protein thiol oxidation in rat liver endoplasmic reticulum. Csala, M., Szarka, A., Margittai, E., Mile, V., Kardon, T., Braun, L., Mandl, J., Bánhegyi, G. Arch. Biochem. Biophys. (2001) [Pubmed]
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