Gentamicin and amikacin repress the growth of Plasmodium falciparum in culture, probably by inhibiting a parasite acid phospholipase.
Human erythrocytes were loaded with either gentamicin or amikacin and subsequently infected with the human malarial parasite Plasmodium falciparum and grown in culture. Parasite invasion of erythrocytes was unaffected by the drugs, but subsequent development was retarded. The digestion of host cell cytosol in ring-stage parasites was inhibited by the drugs. A substantial acid, Ca2+-independent phospholipase activity could be monitored in parasite cytosol and was found to be inhibited by the drugs. These results imply that phospholipases are involved in the feeding mechanism of the parasite and that gentamicin and amikacin exert their inhibitory activity by affecting these enzymes.
D000583:Amikacin / Q000494:pharmacology*; D000962:Antimalarials / Q000494:pharmacology*; D004912:Erythrocytes / Q000469:parasitology; D005839:Gentamicins / Q000494:pharmacology*; D006801:Humans; D010740:Phospholipases / Q000037:antagonists & inhibitors*; D010741:Phospholipases A / Q000037:antagonists & inhibitors*; D010963:Plasmodium falciparum / Q000187:drug effects*
D000962:Antimalarials; D005839:Gentamicins; D000583:Amikacin; D010740:Phospholipases; D010741:Phospholipases A