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Ethanol-induced apoptosis in human HL-60 cells
1Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson 39216-4505, USA.
Life Sciences
|January 1, 1997
Summary
Chronic ethanol use may decrease monocyte counts by inducing apoptosis, a programmed cell death. Inhibiting protein kinase C activity further enhances this ethanol-induced apoptosis in immune cells.
Area of Science:
- Immunology
- Cell Biology
- Toxicology
Background:
- Chronic ethanol abuse is linked to immune dysfunction, notably reduced monocyte numbers.
- The precise mechanisms driving these immune alterations in chronic alcohol users are not fully understood.
Purpose of the Study:
- To investigate whether ethanol induces apoptosis in human promyelocytic leukemia (HL-60) cells.
- To explore the role of protein kinase C in ethanol-induced apoptosis.
Main Methods:
- Human HL-60 cells were treated with ethanol.
- Apoptosis was assessed through DNA fragmentation, phosphatidylserine expression, and cell cycle analysis via flow cytometry.
- The effect of a protein kinase C inhibitor (GF 109203X) on ethanol-induced apoptosis was evaluated.
Main Results:
- Ethanol treatment for 4 days induced characteristic features of apoptosis in HL-60 cells.
- These features included increased DNA fragmentation and phosphatidylserine expression.
- Ethanol also led to a hypodiploid apoptotic cell population, confirmed by flow cytometry.
- Inhibition of protein kinase C potentiated ethanol-induced apoptosis.
Conclusions:
- Ethanol directly induces apoptosis in human HL-60 cells.
- Inhibiting protein kinase C activity enhances ethanol-induced apoptosis.
- These findings offer a partial explanation for ethanol's cytotoxic effects on hematopoietic progenitor cells and link protein kinase C inhibition to ethanol-induced cell death.