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Related Concept Videos

Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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: May 21, 2026

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis
05:30

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis

Published on: November 14, 2025

Cadmium activates a programmed, lysosomal membrane permeabilization-dependent necrosis pathway.

Barbara Messner1, Christian Ploner, Günther Laufer

  • 1Surgical Research Laboratories - Cardiac Surgery, Department of Surgery, Medical University of Vienna, Vienna, Austria. Barbara.Messner@meduniwien.ac.at

Toxicology Letters
|June 9, 2012
PubMed
Summary

Cadmium exposure triggers lysosomal damage and DNA degradation in endothelial cells, leading to programmed necrosis. Overexpressing BCL-XL protein prevents this cell death pathway.

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Studying Copper Nanoparticle-Induced Programmed Cell Death in Bacteria
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Studying Copper Nanoparticle-Induced Programmed Cell Death in Bacteria

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Last Updated: May 21, 2026

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis
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Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis

Published on: November 14, 2025

Studying Copper Nanoparticle-Induced Programmed Cell Death in Bacteria
08:22

Studying Copper Nanoparticle-Induced Programmed Cell Death in Bacteria

Published on: May 16, 2025

Area of Science:

  • Toxicology
  • Cell Biology
  • Pathophysiology

Background:

  • Cadmium (Cd) is a toxic, carcinogenic, and atherogenic element.
  • Cd-induced cell death is a key factor in its toxicity, with previous studies suggesting various mechanisms like apoptosis, necrosis, and autophagy.
  • Endothelial cells (ECs) are crucial for vascular health, and understanding Cd's impact on them is vital.

Purpose of the Study:

  • To precisely define the end-stage processes and outcome of cadmium-induced cell death in endothelial cells.
  • To elucidate the specific mechanisms by which cadmium induces cell death in ECs.
  • To differentiate Cd-induced cell death from other known cell death pathways.

Main Methods:

  • Cd exposure in endothelial cells.
  • Analysis of lysosomal integrity and function (acidification, permeabilization).
  • Detection of DNAse II release and DNA degradation.
  • Measurement of lactate dehydrogenase (LDH) release as a marker of plasma membrane rupture.
  • Genetic manipulation using lentivirus to overexpress the anti-apoptotic protein BCL-XL.

Main Results:

  • Cadmium exposure causes lysosomal acidification and permeabilization.
  • Active DNAse II is released from lysosomes, leading to DNA degradation.
  • Massive release of lactate dehydrogenase (LDH) indicates plasma membrane rupture and necrosis.
  • Overexpression of BCL-XL significantly inhibits lysosomal rupture, DNA degradation, and LDH release.

Conclusions:

  • Cadmium induces a specific programmed cell death pathway in endothelial cells.
  • This pathway is characterized by lysosomal damage and culminates in necrosis.
  • The findings clarify previous misinterpretations of Cd-induced cell death and highlight BCL-XL as a potential protective factor.