Plasmodium mitochondrial inner membrane (MIM)

The Plasmodium mitochondrial inner membrane is a critical site for parasite survival, housing the electron transport chain (ETC) and essential metabolic enzymes. Unlike human mitochondria, which primarily use the ETC for ATP production via oxidative phosphorylation, Plasmodium parasites rely on the ETC mainly to regenerate ubiquinone. This ubiquinone is a vital electron acceptor for dihydroorotate dehydrogenase (DHODH), an enzyme essential for de novo pyrimidine biosynthesis, as the parasite cannot salvage preformed pyrimidines. Consequently, disrupting mitochondrial function or the integrity of the inner membrane leads to a halt in DNA synthesis and parasite death. This system is a validated therapeutic target, most notably addressed by the drug atovaquone, which targets the cytochrome bc1 complex. However, the term as provided is considered 'incorrect' for a specific target entry because it describes a cellular compartment and a broad biological process rather than a single protein or receptor.

Other names

Plasmodium mitochondrial electron transport chainMitochondrial respiratory chainPlasmodium falciparum mitochondrial inner membraneMitochondrial function

Inhibition of essential mitochondrial enzymes such as Cytochrome bc1 complex (Complex III) or Dihydroorotate dehydrogenase (DHODH), leading to the collapse of the mitochondrial membrane potential and cessation of pyrimidine synthesis.