Component
Intracellular chloride concentration in leukemia cells
Chloride loading and associated cell-size and membrane-potential change.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Ivermectin increased intracellular chloride concentration and cell size in leukemia cells, accompanied by plasma membrane hyperpolarisation without a change in mitochondrial membrane potential.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Acute myeloid leukemia cell lines and primary patient samples
- exposure
- Low micromolar ivermectin
- limitations
- The mitochondrial membrane potential was explicitly unchanged, which separates this from mechanisms that act through mitochondrial depolarisation.
- organism
- Acute myeloid leukemia cell lines and primary patient samples
- plain_language
- Ivermectin increased intracellular chloride concentration and cell size in leukemia cells, accompanied by plasma membrane hyperpolarisation without a change in mitochondrial membrane potential.
- primary_references
- The antiparasitic agent ivermectin induces chloride-dependent membrane hyperpolarization and cell death in leukemia cells. (2010). https://pubmed.ncbi.nlm.nih.gov/20644115/ DOI: 10.1182/blood-2010-01-262675
- route
- In vitro
- tissue
- Chloride flux and membrane potential
Ivermectin: mechanism of action across parasite, host barrier and mammalian targets (2026-09-22) · lines 178–187
Original AI-assisted curation of sixteen primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Study-specific citations, concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft
## ivermectin-leukemia-chloride-influx Ivermectin increased intracellular chloride concentration and cell size in leukemia cells, accompanied by plasma membrane hyperpolarisation without a change in mitochondrial membrane potential. Model/species: Acute myeloid leukemia cell lines and primary patient samples Tissue/system: Chloride flux and membrane potential Exposure: Low micromolar ivermectin Route: In vitro Duration: Not stated here Limits: The mitochondrial membrane potential was explicitly unchanged, which separates this from mechanisms that act through mitochondrial depolarisation. Primary reference: The antiparasitic agent ivermectin induces chloride-dependent membrane hyperpolarization and cell death in leukemia cells. (2010). https://pubmed.ncbi.nlm.nih.gov/20644115/ DOI: 10.1182/blood-2010-01-262675 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
Complete structured claim and evidence
Where it participates (unsigned role)
Ivermectin increased reactive oxygen species generation in leukemia cells, and that increase was functionally required for ivermectin-induced cell death.
Experimental context and source evidence
- duration
- Not stated here
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Acute myeloid leukemia cell lines and primary patient samples, with three mouse leukemia models
- exposure
- Low micromolar ivermectin; mouse dosing described as appearing pharmacologically achievable
- limitations
- Death was preferential for leukemia cells over normal hematopoietic cells rather than exclusive to them, and synergy was reported with cytarabine and daunorubicin, which also raise reactive oxygen species.
- organism
- Acute myeloid leukemia cell lines and primary patient samples, with three mouse leukemia models
- plain_language
- Ivermectin increased reactive oxygen species generation in leukemia cells, and that increase was functionally required for ivermectin-induced cell death.
- primary_references
- The antiparasitic agent ivermectin induces chloride-dependent membrane hyperpolarization and cell death in leukemia cells. (2010). https://pubmed.ncbi.nlm.nih.gov/20644115/ DOI: 10.1182/blood-2010-01-262675
- route
- In vitro and in vivo
- tissue
- Reactive oxygen species and cell viability
Ivermectin: mechanism of action across parasite, host barrier and mammalian targets (2026-09-22) · lines 189–198
Original AI-assisted curation of sixteen primary studies resolved by PubMed title search and cross-checked against live PubMed metadata. Study-specific citations, concentrations, negative findings and limitations retained. Not publisher full text. · supports · · source_derived_draft · unverified_draft
## ivermectin-leukemia-reactive-oxygen Ivermectin increased reactive oxygen species generation in leukemia cells, and that increase was functionally required for ivermectin-induced cell death. Model/species: Acute myeloid leukemia cell lines and primary patient samples, with three mouse leukemia models Tissue/system: Reactive oxygen species and cell viability Exposure: Low micromolar ivermectin; mouse dosing described as appearing pharmacologically achievable Route: In vitro and in vivo Duration: Not stated here Limits: Death was preferential for leukemia cells over normal hematopoietic cells rather than exclusive to them, and synergy was reported with cytarabine and daunorubicin, which also raise reactive oxygen species. Primary reference: The antiparasitic agent ivermectin induces chloride-dependent membrane hyperpolarization and cell death in leukemia cells. (2010). https://pubmed.ncbi.nlm.nih.gov/20644115/ DOI: 10.1182/blood-2010-01-262675 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.