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Oxidative haemolysis in protein malnutrition
Clinica Chimica Acta; International Journal of Clinical Chemistry
|October 26, 1981
Summary
Protein-energy malnutrition (PEM) in Kivu causes hemolytic anemia by decreasing erythrocyte resistance to oxidative stress. Reduced activities of glutathione peroxidase and superoxide dismutase likely contribute to shortened red blood cell lifespan in PEM patients.
Area of Science:
- Hematology
- Nutritional Science
- Biochemistry
Background:
- Protein-energy malnutrition (PEM) is associated with various health complications.
- Hemolytic anemia is a recognized complication in severe malnutrition.
- Oxidative stress plays a role in red blood cell damage.
Purpose of the Study:
- To investigate the oxidative status of erythrocytes in patients with PEM in Kivu.
- To identify specific erythrocyte enzyme activities affected by PEM.
- To explore the potential mechanisms underlying hemolytic anemia in PEM.
Main Methods:
- Assessed in vitro resistance of erythrocytes to oxidative stress using acetylphenylhydrazine.
- Measured activities of key erythrocyte enzymes: glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, glutathione reductase, glutathione peroxidase, and superoxide dismutase.
- Quantified levels of reduced glutathione.
Main Results:
- Erythrocytes from PEM patients showed decreased resistance to oxidative aggression, with increased Heinz body formation.
- Activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and glutathione reductase were normal or increased.
- Reduced activities were observed for glutathione peroxidase and superoxide dismutase, enzymes containing trace elements.
Conclusions:
- Shortened erythrocyte lifespan in PEM patients is likely due to an oxidative process.
- Decreased activities of glutathione peroxidase and superoxide dismutase contribute to this oxidative stress.
- Trace element depletion is hypothesized as a potential cause for the reduced activity of these enzymes.