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Red cell damage induced by peroxidized microsomes: the relationship between hemolytic activity and peroxide content
M Pesh-Imam1, R J Willis, R O Recknagel
1Department of Physiology, School of Medicine, Case Western Reserve University, Cleveland, Ohio.
Journal of Environmental Science and Health. Part C: Environmental Health Sciences
|January 1, 1978
Summary
Rat liver microsomes initiate lipid peroxidation, generating a toxic factor that damages red blood cells. This study isolates the hemolytic component, demonstrating it
Area of Science:
- Biochemistry
- Toxicology
- Cell Biology
Background:
- NADPH-initiated lipid peroxidation in rat liver microsomes causes red blood cell hemolysis in vitro.
- A non-radical toxic factor generated from peroxidizing microsomal lipids causes prelytic damage to red blood cells.
Purpose of the Study:
- To demonstrate that the microsomal lipid peroxidation step can be separated from the subsequent hemolytic attack on red blood cells.
- To identify and characterize the lipoidal component responsible for hemolysis.
Main Methods:
- Calcium-aggregated rat liver microsomes were peroxidized and then centrifuged.
- Resuspended peroxidized microsomes and extracted lipids were tested for hemolytic activity.
- Hemolytic activity and lipid peroxide generation were monitored over time.
Main Results:
- Peroxidized microsomes caused hemolysis even after separation from the peroxidation process.
- Lipids extracted from peroxidized microsomes quantitatively accounted for the hemolytic activity.
- Hemolytic activity peaked at 20 minutes, correlating with peak lipid-soluble peroxide generation.
Conclusions:
- A separable lipoidal factor derived from microsomal lipid peroxidation is responsible for red blood cell hemolysis.
- The generation and activity of this hemolytic factor are time-dependent and correlate with lipid peroxide levels.