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Published on: August 14, 2013
Effects of ascorbic acid on glucose-6-phosphate dehydrogenase-deficient erythrocytes: studies in an animal model
Insights
High doses of ascorbic acid may harm red blood cells in individuals with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. This study shows ascorbic acid causes premature destruction of G-6-PD-deficient erythrocytes in rats.
Area of Science:
- Biochemistry
- Hematology
- Pharmacology
Background:
- Limited data exists on ascorbic acid's impact on glucose-6-phosphate dehydrogenase (G-6-PD)-deficient erythrocytes.
- G-6-PD deficiency is a common genetic disorder affecting red blood cell metabolism.
Purpose of the Study:
- To investigate the effects of ascorbic acid on the survival of G-6-PD-deficient erythrocytes.
- To determine if ascorbic acid administration poses a risk to individuals with G-6-PD deficiency.
Main Methods:
- Studied the survival of 51Cr-labeled G-6-PD-deficient erythrocytes incubated with ascorbic acid in rats.
- Rats were pretreated to create partial reticuloendothelial and complement blockade.
- Compared survival rates of G-6-PD-deficient cells (with and without ascorbic acid) against normal erythrocytes.
Main Results:
- Ascorbic acid significantly impaired the survival of G-6-PD-deficient erythrocytes.
- G-6-PD-deficient cells survived normally when not incubated with ascorbic acid.
- Ascorbic acid did not affect the survival of normal erythrocytes at tested concentrations.
Conclusions:
- Ascorbic acid can cause premature destruction of G-6-PD-deficient erythrocytes.
- Caution is advised when administering high doses of ascorbic acid to potentially G-6-PD-deficient individuals.
- Further clinical and experimental studies are warranted to confirm these findings in humans.
Abstract:
There is little information available concerning the possible effects of ascorbic acid on glucose-6-phosphate dehydrogenase (G-6-PD) -deficient erythrocytes. We therefore studied the survival of G-6-PD-deficient cells, incubated with ascorbic acid, in rats with partial reticuloendothelial and complement blockade. Animals were pretreated with ethyl palmitate and cobra venom factor. They were then transfused with 51Cr-labeled erythrocytes which had been incubated in the presence or absence of ascorbic acid. G-6-PD-deficient cells, incubated with ascorbic acid, had impaired survival when compared to that of controls. G-6-PD-deficient cells, in the absence of ascorbic acid, had survival times equal to those of normal control erythrocytes. At the concentrations used, ascorbic acid did not appear to alter the survival of normal cells. Ascorbic acid causes premature loss of G-6-PD-deficient human erythrocytes in this rat model. On the basis of previous clinical and experimental observations, as well as this study, caution should be used when administering ascorbic acid in large doses to individuals who might be G-6-PD deficient.
