Related Experiment Video
Updated: Aug 2, 2026

A Simple Protocol for Platelet-mediated Clumping of Plasmodium falciparum-infected Erythrocytes in a Resource Poor Setting
Published on: May 16, 2013
Oxidative stress and rheology in severe malaria
A M Dondorp1, F Omodeo-Salè, K Chotivanich
1Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. AMDondorp@Yahoo.com
Abstract:
There is mounting evidence that the release of haemozoin (beta-haematin), which is produced in large amounts during malaria infection and is released into the circulation during schizont rupture, is associated with damage to cell membranes through an oxidative mechanism. The red blood cell membrane is thus oxidised, causing rigidity of the cell. This can contribute to the pathophysiology of severe malaria, since red blood cells will have to deform considerably in order to squeeze through the microcirculation, the patency of which is disturbed by sequestered red blood cells containing the mature forms of the parasite. Rigidity of red blood cells forms a new target for intervention. Since this seems to be caused by oxidative damage to the red blood cell membrane, the anti-oxidant N-acetylcysteine is a promising candidate for adjunctive treatment in severe malaria, which still has a mortality rate as high as 20%.
Insights
Malaria infection releases haemozoin, causing oxidative damage and red blood cell rigidity. The antioxidant N-acetylcysteine shows promise for treating severe malaria by protecting against this cellular damage.
Area of Science:
- Biochemistry
- Pathophysiology
- Pharmacology
Background:
- Haemozoin (beta-haematin) release during malaria infection is linked to oxidative damage.
- Oxidative stress damages red blood cell membranes, increasing cell rigidity.
- This rigidity contributes to severe malaria pathophysiology by impeding microcirculation.
Purpose of the Study:
- To investigate the role of haemozoin-induced oxidative damage in red blood cell rigidity.
- To evaluate N-acetylcysteine as a potential adjunctive therapy for severe malaria.
Main Methods:
- Review of evidence linking haemozoin release to oxidative mechanisms.
- Analysis of the impact of red blood cell membrane oxidation on cell deformability.
- Consideration of N-acetylcysteine's antioxidant properties in the context of malaria.
Main Results:
- Haemozoin release causes oxidative damage to red blood cell membranes.
- Oxidized red blood cells become rigid, hindering microcirculation.
- This rigidity represents a potential therapeutic target in severe malaria.
Conclusions:
- Oxidative damage to red blood cells is a key factor in severe malaria.
- N-acetylcysteine's antioxidant capacity makes it a promising adjunctive treatment.
- Targeting red blood cell rigidity could improve outcomes in severe malaria.
More Related Videos
10:22Methods to Investigate the Regulatory Role of Small RNAs and Ribosomal Occupancy of Plasmodium falciparum
Published on: December 4, 2015
09:04In Vivo Tracking of Edema Development and Microvascular Pathology in a Model of Experimental Cerebral Malaria Using Magnetic Resonance Imaging
Published on: June 8, 2017
Related Concept Videos
Malaria
Hemorrhagic Stroke ll: Pathophysiology