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The Intrinsic Apoptotic Pathway

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 Autophagy

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...

Apoptosis

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.

Cellular Injury IV: Necrosis

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

Phagocytosis of Apoptotic Cells

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
Normal cells contain receptors that prevent them from being recognized by phagocytes.

The Extrinsic Apoptotic Pathway

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...

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Related Experiment Video

Updated: Jul 18, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Intracellular redox changes during apoptosis.

A F Slater¹, C Stefan, I Nobel

¹Institute of Environmental Medicine, Karolinska Institute, Sweden.

Cell Death and Differentiation

|January 1, 1996

Summary

Apoptosis involves proteases like ICE, but oxidative stress isn't always required. Glutathione (GSH) depletion via efflux, not oxidation, may explain oxidative damage during cell death.

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Last Updated: Jul 18, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

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Published on: June 29, 2011

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

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Published on: February 16, 2015

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor

Published on: April 1, 2011

Area of Science:

Cell Biology
Biochemistry
Molecular Biology

Background:

Apoptosis involves ICE-like proteases and downstream events like cell shrinkage.
Oxidative stress can induce apoptosis, but the mechanism is unclear.
Oxidative modifications are observed in apoptosis, yet reactive oxygen species requirement is debated.

Purpose of the Study:

To investigate the role of oxidative stress and glutathione in apoptosis.
To clarify the mechanism linking oxidative damage to apoptosis.
To explain contradictory findings regarding antioxidants and oxidative products in apoptosis.

Main Methods:

Studied JURKATT lymphocytes treated with Fas/APO-1 antibodies.
Measured intracellular reduced glutathione (GSH) levels and efflux.
Analyzed oxidative modifications in apoptotic cells.

Main Results:

Apoptosis was accompanied by a depletion of intracellular GSH.
GSH depletion resulted from accelerated efflux, not intracellular oxidation.
Oxidative damage to proteins and lipids occurred without increased oxidant production.

Conclusions:

GSH efflux, a non-oxidative mechanism, leads to loss of cellular reducing environment.
This GSH efflux explains oxidative damage and antioxidant effects in apoptosis.
Apoptosis can proceed with oxidative damage without a primary increase in oxidants.