Apigeninidin chloride disrupts Toxoplasma gondii Mitochondrial membrane potential and induce reactive oxygen species and metabolites production

These metabolites are associated with lipid, protein, and nucleic acid disruptions. Using atovaquone (Atov) as a control, we observed that it disrupted intracellular tachyzoites' mitochondrial membrane potential, increased ROS and MitoSOX production, and altered metabolite and lipid production similar to what was observed with our experimental compound APi. Overall, our results indicated that APi targets <i>T. gondii</i> tachyzoite growth through inducing oxidative stress, mitochondrial dysfunction, and eventually parasite death.