Abstract
The intraerythrocytic malaria parasite is under constant oxidative stress originating both from endogenous and exogenous processes. The parasite is endowed with a complete network of enzymes and proteins that protect it from those threats, but also uses redox activities to regulate enzyme activities. In the present analysis, the transcription of the genes coding for the antioxidant defense elements are viewed in the time-frame of the intraerythrocytic cycle. Time-dependent transcription data were taken from the transcriptome of the human malaria parasite Plasmodium falciparum. Whereas for several processes the transcription of the many participating genes is coordinated, in the present case there are some outstanding deviations where gene products that utilize glutathione or thioredoxin are transcribed before the genes coding for elements that control the levels of those substrates are transcribed. Such insights may hint to novel, non-classical pathways that necessitate further investigations.
Highlights
The Plasmodium-infected erythrocyte is under constant oxidative stress
This is caused by exogenous reactive oxidant species (ROS) and reactive nitrogen species (RNS) produced by the immune system of the host, and by endogenous production of ROS generated during the digestion of host cell haemoglobin and concomitant biochemical reactions
These events start to happen at the late ring-early trophozoite stage when the parasite engages in intensive digestion of the host cell haemoglobin and the surface of the erythrocyte is sufficiently altered to be recognized by the reticuloendothelial system as 'non-self'
Summary
The Plasmodium-infected erythrocyte is under constant oxidative stress. This is caused by exogenous reactive oxidant species (ROS) and reactive nitrogen species (RNS) produced by the immune system of the host, and by endogenous production of ROS generated during the digestion of host cell haemoglobin and concomitant biochemical reactions. The entire battery of antioxidant enzymes and their substrates must be functionally present when the parasite starts the digestion of host cell haemoglobin and when the immune system starts to be challenged by parasite antigens. Some ROS may escape the antioxidant defense of the parasite and reach the host erythrocyte where they are handled by catalase and glutathione peroxidase. Even this defense system is not fully effective since the fingerprints of oxidative stress are discernable in the membrane of the infected red blood cells (RBC) such as clustering of band 3 [6] and increased levels of lipid peroxides [7]. The stage-dependent transcription of genes that code for enzymes and proteins that are involved in (page number not for citation purposes)
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