Study summary · research use only
Effect of the mitochondrial uncoupling agent BAM15 against the Toxoplasma gondii RH strain and Prugniaud strain
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study examined the mitochondrial uncoupling agent BAM15 against Toxoplasma gondii RH and Prugniaud (PRU) strains, using in vitro assays (including Vero cells) and in vivo experiments in mice. The abstract reports an EC50 of 1.25 μM for BAM15 against T. gondii in vitro, alongside an IC50 of 27.07 μM in Vero cells. BAM15 treatment was associated with inhibited proliferation of both T. gondii strains, parasite death, mitochondrial vacuolation and autolysis observed by electron microscopy, decreased mitochondrial membrane potential and ATP levels, and increased reactive oxygen species. The authors describe BAM15 as a mitochondrial inhibitor of T. gondii that may serve as a lead molecule for developing therapeutic mitochondrial inhibitors in toxoplasmosis.
Abstract
Toxoplasmosis is a zoonotic disease caused by the infection of the protozoa Toxoplasma gondii (T. gondii), and safe and effective therapeutic drugs are lacking. Mitochondria, is an important organelle that maintains T. gondii survival, however, drugs targeting mitochondria are lacking. The cytotoxicity of BAM15 was detected by CCK-8 and the in vitro effects of BAM15 was detected by qPCR, plaque assay and flow cytometry. Furthermore, the ultrastructural changes of T. gondii after BAM15 treatment were observed by transmission electron microscopy, and further the mitochondrial membrane potential (ΔΨm), ATP level and reactive oxygen species (ROS) of T. gondii after BAM15 treatment were detected. The pharmacokinetic experiments and in vivo infection assays were performed in mice to determine the in vivo effect of BAM15. BAM15 had excellent anti-T. gondii activity in vitro and in vivo with an EC50 value of 1.25 μM, while the IC50 of BAM15 in Vero cells was 27.07 μM. Notably, BAM15 significantly inhibited proliferation activity of T. gondii RH strain and Prugniaud strain (PRU), caused T. gondii death. Furthermore, BAM15 treatment induced T. gondii mitochondrial vacuolation and autolysis by TEM. Moreover, the decrease in ΔΨm and ATP level, as well as the increase in ROS production further confirmed the changes CONCLUSIONS: Our study identifies a useful T. gondii mitochondrial inhibitor, which may also serve as a leading molecule to develop therapeutic mitochondrial inhibitors in toxoplasmosis.'
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