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The mitochondrial membrane potential (ΔΨm) in trypanosomes, specifically in the bloodstream form of Trypanosoma brucei, is a crucial electrochemical gradient across the inner mitochondrial membrane. Unlike most eukaryotes, bloodstream form trypanosomes primarily generate ΔΨm through ATP hydrolysis by the reverse operation of FoF1-ATP synthase, as they lack cytochromes and do not perform classical oxidative phosphorylation. Maintaining ΔΨm is essential for parasite viability, driving import/export processes, and supporting organelle homeostasis. Disrupting this potential leads to cell dysfunction and death, making it a relevant target for anti-trypanosomal therapies.
Disruption of FoF1-ATP synthase activity, leading to collapse of mitochondrial membrane potential.
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