Related Experiment Video
Updated: Jun 20, 2026

12:55
Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
Published on: February 16, 2015
Ethanol induces apoptosis in human mast cells.
Life Sciences
|September 25, 2009
Summary
Ethanol significantly reduces mast cell viability and proliferation, leading to apoptosis. This finding helps explain how alcohol abuse weakens the immune system, increasing infection risk.
Area of Science:
- Immunology
- Cell Biology
Background:
- Alcohol abuse is linked to increased infections due to immune suppression.
- The exact mechanisms of ethanol-induced immune suppression remain unclear.
- Mast cells (MC) are crucial innate immune cells involved in host defense.
Purpose of the Study:
- To investigate the impact of ethanol and acetaldehyde on mast cell viability, proliferation, and apoptosis.
- To elucidate the cellular and molecular mechanisms underlying ethanol's effects on mast cells.
Main Methods:
- Utilized human mast cell line (HMC)-1, mouse bone marrow-derived mast cells (mBMMC), and human peripheral blood-derived mast cells (HuMC).
- Assessed proliferation via [(3)H]thymidine incorporation and trypan blue exclusion.
- Evaluated apoptosis using nucleosome measurements, caspase activity assays (caspase-3, -8, -9), Tunel assay, and analysis of Bcl-2/Bax protein expression.
Main Results:
- Ethanol, but not acetaldehyde, inhibited mast cell proliferation and viability in a dose-dependent manner.
- Ethanol induced apoptotic cell death in HMC-1 cells at concentrations as low as 43mM.
- Apoptosis induction correlated with increased caspase-3 activity and altered Bcl-2/Bax protein expression, favoring apoptosis.
Conclusions:
- Ethanol significantly reduces mast cell viability through apoptosis.
- The observed decrease in mast cell viability may contribute to the immunosuppression associated with chronic ethanol abuse.
- Understanding these mechanisms is vital for addressing the health consequences of alcohol consumption.
Related Concept Videos
Apoptosis
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
The Extrinsic Apoptotic Pathway
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Cellular Injury V: Apoptosis and Autophagy
Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
The Intrinsic Apoptotic Pathway
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
