that incorporation of labeled purines into DNA begins approximately 30 hours after merozoite invasion and increases logarithmically for another 14 to 18 hours, when schizogony is completed.

Because erythrocytes contain considerable concentrations of amino acids and vitamins that may be important to parasite development, it is difficult to determine in experimental settings whether decreased parasite viability due to nutritional factors is a result of effects on the parasite itself or on the red blood cell. Thus, it is not known whether nutrients identified as crucial for malaria parasite cultivation are required for erythrocytes only, parasites only, or both. For example, the amino acids glutamine, glycine, and cysteine, while necessary for long-term survival of erythrocytes in culture, may not be required parasite nutrients.

Energy Transformations and Mitochondria

There has been considerable debate about whether the erythrocytic stages of mammalian malaria parasites possess mitochondria, the energy-producing organelles essential for all life forms. The falciparum parasite uses glucose as its primary energy source. In fact, glucose utilization is significantly greater in the infected erythrocyte than in the uninfected cell. Progress is being made in the characterization of the enzymes involved in glycolysis in P. falciparum (Roth et al., 1988; Roth, 1990). However, there is no evidence supporting the presence of a Krebs cycle, a key energy-producing process of the mitochondria.

The presence of mitochondria in the erythrocytic asexual stages of P. falciparum has recently been shown, but their actual function is not well understood (Divo et al., 1985b). Recent advances in the molecular biology of the mitochondrial DNA of malaria parasites may help to unravel the role of the mitochondrion (Gardner et al., 1988). The importance of this organelle to the parasite is underscored by the fact that mitochondrial toxins are highly lethal. Antibiotics used to treat falciparum infection, such as the tetracyclines, clindamycin, and erythromycin, appear to work by blocking the development of parasite mitochondria (Prapunwattana et al., 1988). Of great interest in this regard is the recent finding that mitochondrial DNA of P. falciparum encodes an RNA polymerase which is closely related to prokaryotic polymerases and is sensitive to rifampicin, potentially explaining the antimalarial activity of this drug (Gardner et al., 1991).

The erythrocytic stages of many mammalian malaria parasites appear not to derive their metabolic energy through classical electron transport. The mitochondria may participate in ion transport, but the role this plays in metabolism is unclear. It is not known whether components analogous to those present in the mammalian terminal electron transport system function in the malaria parasite, and for what purpose, since the organism, like many

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