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.
Csala
M
M
Department of Medical Chemistry, Semmelweis University, Budapest, Hungary.
Szarka
A
A
Margittai
E
E
Mile
V
V
Kardon
T
T
Braun
L
L
Mandl
J
J
Bánhegyi
G
G
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism*; D004583:Electrons; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism*; D008954:Models, Biological; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds / Q000378:metabolism*; D013997:Time Factors; D014810:Vitamin E / Q000502:physiology*; D014811:Vitamin E Deficiency / Q000378:metabolism
D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds; D014810:Vitamin E; D001205:Ascorbic Acid