ArticleParasitology research2019
G418 induces programmed cell death in Acanthamoeba through the elevation of intracellular calcium and cytochrome c translocation.
Article in Parasitology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Amebicidal Effect of Adamantane-Azole Gold(I) Complexes: Cell Death Mechanisms and Synergistic Action with Chlorhexidine againstACS omega · 2026Article
- Alternative splicing drives a dynamic transcriptomic response duringMicrobial cell (Graz, Austria) · 2025Article
- Alpha-Mangostin and its nano-conjugates induced programmed cell death in Acanthamoeba castellanii belonging to the T4 genotype.International microbiology : the official journal of the Spanish Society for Microbiology · 2024Article
- Effect of embelin on inhibition of cell growth and induction of apoptosis in Acanthamoeba castellanii.Archives of microbiology · 2023Article
- Article
- Opportunistic free-living amoebal pathogens.Pathogens and global health · 2022Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acanthamoeba is a widely distributed opportunistic parasite which causes a vision-threatening keratitis and a life-threatening encephalitis. The cyst stage of this amoeba is especially resistant to currently used therapeutics and so alternative agents are urgently required. Growing evidence supports the existence of a programmed cell death system (PCD) in Acanthamoeba and while some features are shared by higher eukaryote cells, others differ. It is hoped that by understanding these differences we can exploit them as targets for novel drug intervention to activate PCD pathways in the amoebae but not the invaded human tissue. Here, we use the aminoglycoside G418 to activate PCD in Acanthamoeba. This drug caused a shape change in the treated amoebae. Cells rounded up and contracted, and after 6 h fragments of cells resembling the 'apoptotic bodies' of vertebrate cells were observed. G418 causes an increase in intracellular calcium from a resting level of 24 nM to 60 nM after 6 h of treatment. Mitochondrial function as assayed by the ΔΨ
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