ArticleScientific reports2016
Oxidative stress generated during monensin treatment contributes to altered Toxoplasma gondii mitochondrial function.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44 citing papers in PubMed, 79 citations in OpenAlex.
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- Oxidative Stress in Parasitic Diseases-Reactive Oxygen Species as Mediators of Interactions between the Host and the Parasites.Antioxidants (Basel, Switzerland) · 2023Review
- ADAMTS-1 has nuclear localization in cells with epithelial origin and leads to decreased cell migration.Experimental cell research · 2023Article
- The vacuolar iron transporter mediates iron detoxification in Toxoplasma gondii.Nature communications · 2023Article
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Authors and funding
2 authors at 2 institutions in 1 country.
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Abstract
The ionophore monensin displays potent activities against several coccidian parasites of veterinary and medical importance including the opportunistic pathogen of humans, Toxoplasma gondii. While monensin is used widely in animals, toxicity impedes its use in humans. Nonetheless, given its potency, understanding its mode of action would reveal vulnerable aspects of the parasite that can be exploited for drug development. We previously established that monensin induces Toxoplasma to undergo cell cycle arrest and an autophagy-like cell death. Interestingly, these effects are dependent on the mitochondrion-localized TgMSH-1 protein, suggesting that monensin disrupts mitochondrial function. We demonstrate that monensin treatment results in decreased mitochondrial membrane potential and altered morphology. These effects are mitigated by the antioxidant compound N-acetyl-cysteine suggesting that monensin causes an oxidative stress, which was indeed the case based on direct detection of reactive oxygen species. Moreover, over-expression of the antioxidant proteins glutaredoxin and peroxiredoxin 2 protect Toxoplasma from the deleterious effects of monensin. Thus, our studies show that the effects of monensin on Toxoplasma are due to a disruption of mitochondrial function caused by the induction of an oxidative stress and implicate parasite redox biology as a viable target for the development of drugs against Toxoplasma and related pathogenic parasites.
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