vitamin-k-1 and Hemolysis

A diurnal variation exists in blood levels of the vitamin K-dependent bone protein osteocalcin. However, it is not known whether the carboxylated and undercarboxylated constituents of osteocalcin also vary. Therefore, osteocalcin and undercarboxylated osteocalcin were measured in specimens collected every 4 hours over a 24-hour period in nine healthy subjects (five males, four females) ages 20-33 years who were consuming a mixed diet containing 100 microg of phylloquinone. Osteocalcin and undercarboxylated osteocalcin were measured by radioimmunoassay (RIA) before and after treatment with barium sulfate. Although the percent undercarboxylated osteocalcin did not change, a diurnal variation was observed in total osteocalcin, carboxylated osteocalcin, and undercarboxylated osteocalcin, with peak concentrations at 4 a.m. and the lowest concentrations between 12 p.m. and 4 p.m. The difference between the total osteocalcin peak and trough concentrations averaged 28 +/- 7 (SEM)%. There were no gender differences in these rhythms. The effect of dietary phylloquinone as a modulator of these rhythms was evaluated in a randomized study by increasing phylloquinone intake to 420 microg/day with fortified corn oil, split between the lunch and dinner meals. Total and carboxylated osteocalcin fluctuations and concentrations were not affected by the dietary treatment. The diurnal variation in undercarboxylated osteocalcin was abolished with supplementation and concentrations at 8 a.m. (14 hours following supplementation) (2.3 +/- 0.2 ng/ml) were significantly lower than the unsupplemented levels (2.7 +/- 0.2 ng/mL, P = 0.006). The percentage of undercarboxylated osteocalcin was similarly decreased after supplementation (19.7 +/- 1.3%) in relation to the mixed diet cycle (24.2 +/- 1.6%, P = 0.006) at 8 a.m. on the second day. Dietary supplementation induced a fluctuation in percentage undercarboxylated osteocalcin with a decline in levels starting at approximately 12 a.m. Therefore, additional dietary phylloquinone does not appear to modulate the total osteocalcin diurnal rhythm, but can influence its undercarboxylated component.

Topics: Adult; Biological Availability; Circadian Rhythm; Diet; Female; Hemolysis; Humans; Male; Osteocalcin; Radioimmunoassay; Vitamin K 1

To determine whether vitamin K1, which is routinely administered to neonates, could act as an exogenous oxidising agent and be partly responsible for haemolysis in glucose-6-phosphat-dehydrogenase (G-6-PD).. G-6-PD deficient (n = 7) and control (n = 10) umbilical cord blood red blood cells were incubated in vitro with a vitamin K1 preparation (Konakion). Two concentrations of Vitamin K1 were used, both higher than that of expected serum concentrations, following routine injection of 1 mg vitamin K1. Concentrations of reduced glutathione (GSH) and methaemoglobin, indicators of oxidative red blood cell damage, were determined before and after incubation, and the mean percentage change from baseline calculated.. Values (mean (SD)) for GSH, at baseline, and after incubation with vitamin K1 at concentrations of 44 and 444 microM, respectively, and percentage change from baseline (mean (SD)) were 1.97 + 0.31 mumol/g haemoglobin, 1.89 +/- 0.44 mumol/g (-4.3 +/- 13.1%), and 1.69 +/- 0.41 mumol/g (-14.5 +/- 9.3%) for the G-6-PD deficient red blood cells, and 2.27 +/- 0.31 mumol/g haemoglobin, 2.09 +/- 0.56 mumol/g (-7.2 +/- 23.2%), and 2.12 +/- 0.38 mumol/g (-6.0 + 14.1%) for the control cells. For methaemoglobin (percentage of total haemoglobin), the corresponding values were 2.01 +/- 0.53%, 1.93 +/- 0.37% (-0.6 +/- 17.4%) and 2.06 +/- 0.43% (5.7 +/- 14.2%) for the G-6-PD deficient red blood cells, and 1.56 +/- 0.74%, 1.70 +/- 0.78% (12.7 +/- 21.9%), and 1.78 +/- 0.71% (20.6 +/- 26.8%) for the control red blood cells. None of the corresponding percentage changes from baseline was significantly different when G-6-PD deficient and control red blood cells were compared.. These findings suggest that G-6-PD deficient red blood cells are not at increased risk of oxidative damage from vitamin K1.

Topics: Biomarkers; Cells, Cultured; Erythrocytes; Glucosephosphate Dehydrogenase Deficiency; Glutathione; Hemolysis; Humans; Infant, Newborn; Male; Methemoglobin; Oxidants; Vitamin K 1

Topics: Anaerobiosis; Animals; Bacteroides; Bacteroides Infections; Culture Media; Erythrocytes; Hemin; Hemolysis; Humans; Sheep; Succinates; Vitamin K; Vitamin K 1

Topics: Amobarbital; Child; Chloramphenicol; Chlorpromazine; Diphenhydramine; Hematuria; Hemolysis; Hydrocortisone; Hypoprothrombinemias; Mephenesin; Meprobamate; Penicillins; Phenobarbital; Promethazine; Purpura; Purpura, Thrombocytopenic; Sulfamethizole; Sulfathiazoles; Tetanus; Tetanus Toxoid; Toxicology; Tracheotomy; Trimeprazine; Tubocurarine; Vitamin K 1

Topics: Aldehydes; Cell Membrane; Cell Membrane Permeability; Electrons; Ergocalciferols; Glycosides; Hemolysis; Hydroquinones; Microscopy; Microscopy, Electron; Oxidation-Reduction; Rabbits; Research; Squalene; Ubiquinone; Vitamin A; Vitamin K; Vitamin K 1; Vitamins

Topics: Administration, Intravenous; Antifibrinolytic Agents; Hemolysis; Hemorrhagic Disorders; Humans; Hypoprothrombinemias; Prothrombin; Vitamin K; Vitamin K 1