Logo image
Back
Mitochondrial and plastid functions as antimalarial drug targets
Journal article

Mitochondrial and plastid functions as antimalarial drug targets

Akhil B Vaidya
Current drug targets. Infectious disorders, v 4(1), pp 11-23
Mar 2004
DOI: https://doi.org/10.2174/1568005043480907
PMID: 15032631

Abstract

Symbiosis Electron Transport Antimalarials - metabolism Humans Antimalarials - therapeutic use Mitochondria - metabolism Mitochondria - drug effects Animals Terpenes - metabolism Cell Nucleus - genetics Chromosomes - genetics Models, Biological Plastids - drug effects Plastids - metabolism Fatty Acids - biosynthesis
Malaria parasites possess three genomes: the nuclear chromosomes, the mitochondrial genome, and the plastid genome. Realization that the parasites contain a plastid remnant with its own genome has created much excitement not only from a basic biological point of view but also from the prospects for developing new antimalarial drugs. Both the mitochondrial and the plastid genomes are the smallest examples of their kind known to date. The plastid appears to be derived from an ancestral secondary endosymbiotic event. Interestingly, the main functions usually associated with a mitochondrion and a plastid, i.e. oxidative phosphorylation and photosynthesis, do not appear to be conserved in malaria parasites. Completion of the parasite genome sequence has provided the opportunity to assess functions assigned to these highly derivatized organelles. It is clear that these organelles serve vital functions since interference with their activity is incompatible with parasite growth. A number of antimalarial compounds target functions of either the mitochondrion or the plastid. This review will survey our current understanding of mitochondrial and plastid functions with a view to identify processes that are or have a potential to be targets for antimalarial drugs.

Metrics

12 Record Views
34 citations in Scopus

Details

Logo image