Abstract
In non fatal and synchronous P. chabaudi rodent malaria, we observed at the stage of parasitaemia peak, an alteration (50 % decrease) in LCAT activity. This decrease could be related partly to hepatic dysfunction, and mainly to circulating inhibitors released into blood from parasitized red blood cells at each end of a schizogonic cycle. This decrease in LCAT activity, at this step of the infection, accounts for part of the dyslipoproteinemia previously observed (i.e., increase in cholesterol and phospholipids into VLDL-LDL and decrease in the EC series and delayed conversion of Tg-rich lipoproteins into LDL-HDL. At a prepatent step of infection and after the parasitaemia peak, the alterations observed in LCAT activity, (respectively, increase and then decrease), would be related to similar changes in levels of cholesterol of HDL associated to complex changes in triacylglyceride transport and metabolism.
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