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Related Concept Videos

Apoptosis01:30

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 Pathway01:17

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...
The Intrinsic Apoptotic Pathway01:31

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...
Cellular Injury V: Apoptosis and Autophagy01:22

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...

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Related Experiment Video

Updated: Jul 12, 2026

Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure
10:07

Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure

Published on: March 20, 2012

Ethanol-induced apoptosis in vitro.

M G Neuman1, N H Shear, R G Cameron

  • 1Division of Clinical Pharmacology, Sunnybrook and Women's College Health Sciences Centre, Toronto, Ontario, Canada. manuela@srcl.sunnybrook.utoronto.ca

Clinical Biochemistry
|December 30, 1999
PubMed
Summary
This summary is machine-generated.

Ethanol (EtOH) exposure induces apoptosis in human liver cells in a dose-dependent manner. Increased EtOH frequency significantly elevates apoptosis, with primary hepatocytes showing higher sensitivity.

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Area of Science:

  • Hepatology
  • Cell Biology
  • Toxicology

Background:

  • Alcohol consumption is a leading cause of liver disease.
  • Ethanol's cytotoxic effects on hepatocytes contribute to liver damage.
  • Understanding the mechanisms of ethanol-induced liver injury is crucial.

Purpose of the Study:

  • To investigate the apoptotic process induced by ethanol in human liver cells.
  • To establish an in vitro model for studying ethanol-induced apoptosis.

Main Methods:

  • Exposure of normal human primary hepatocytes (HPH) and Hep G2 cells to varying ethanol concentrations.
  • Analysis of 6000 cells per sample using transmission electron microscopy.
  • Quantification of apoptotic cell percentages at different ethanol doses and exposure frequencies.

Main Results:

  • Ethanol exposure significantly increased apoptosis in a dose-dependent manner (e.g., 80 mmol/L EtOH resulted in 26% apoptosis, p < 0.001).
  • Repeated ethanol exposure (two consecutive doses of 80 mmol/L) markedly elevated apoptosis to 55% (p < 0.0001).
  • Normal human primary hepatocytes exhibited stronger apoptotic activity compared to Hep G2 cells (p < 0.05).

Conclusions:

  • Ethanol-induced apoptosis in vitro is regulated by both the dose and frequency of exposure.
  • Human primary hepatocytes are more susceptible to ethanol-induced apoptosis than Hep G2 cells.
  • This study provides insights into the cellular mechanisms of alcohol-related liver disease.