Participants In Vitamin Research Articles

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.

The metabolic functions of vitamin B 12: II. Participation of vitamin B 12 in the biosynthesis of deoxyribonucleic acid and its acid-soluble precursors

Addition of excess vitamin B 12 to previously limited cultures of Lactobacillus leichmannii increased the concentration of DNA, the ratios DNA/RNA and DNA/ protein, and the concentration per milligram of protein of acid-soluble deoxyribosides dexoyribonucleotides and unidentified compounds containing deoxyribosyl moieties in combined form. Time-course studies of the appearances of the acid-soluble deoxyriboysl compounds favor the hypothesis that they are DNA precursors and that vitamin B 12 functions primarily in their biosynthesis. The results also provide additional information on the unbalanced growth state resulting from vitamin B 12 or deoxyriboside deprivation. If nutritional repletion takes place after more than 2 h of unbalanced growth in deficient media, filamentous growth is not fully reversed despite extensive replacement of DNA.