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Effect of vitamin K1 on glucose-6-phosphate dehydrogenase deficient neonatal erythrocytes in vitro
1Department of Pediatrics, Shaare Zedek Medical Centre, Jerusalem, Israel. kaplan@cc.huji.ac.il
Insights
Vitamin K1 does not increase oxidative damage in glucose-6-phosphatase dehydrogenase (G-6-PD) deficient red blood cells. This study found no significant difference in red blood cell damage between G-6-PD deficient and control cells when exposed to vitamin K1.
Area of Science:
- Hematology
- Biochemistry
- Neonatal Medicine
Background:
- Vitamin K1 is routinely given to newborns.
- Glucose-6-phosphatase dehydrogenase (G-6-PD) deficiency is a common genetic disorder.
- Oxidative stress can cause hemolysis in G-6-PD deficient red blood cells.
Purpose of the Study:
- To investigate if vitamin K1 acts as an oxidizing agent.
- To determine if vitamin K1 contributes to hemolysis in G-6-PD deficient neonates.
Main Methods:
- Incubation of G-6-PD deficient and control red blood cells with vitamin K1 in vitro.
- Measurement of reduced glutathione (GSH) and methaemoglobin levels.
- Calculation of percentage change from baseline for oxidative stress indicators.
Main Results:
- No significant difference in GSH levels between G-6-PD deficient and control cells after vitamin K1 incubation.
- No significant difference in methaemoglobin levels between G-6-PD deficient and control cells after vitamin K1 incubation.
- Vitamin K1 did not cause a significantly greater oxidative damage in G-6-PD deficient red blood cells compared to controls.
Conclusions:
- G-6-PD deficient red blood cells are not at increased risk of oxidative damage from vitamin K1.
- Routine vitamin K1 administration in neonates is unlikely to cause hemolysis in G-6-PD deficient infants due to oxidative stress.
Aim:
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).
Methods:
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.
Results:
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.
Conclusions:
These findings suggest that G-6-PD deficient red blood cells are not at increased risk of oxidative damage from vitamin K1.