Related Experiment Video

Updated: Oct 3, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles
08:35

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Published on: October 5, 2012

Attenuation of both apoptotic and necrotic actions of cadmium by Bcl-2

Masami Ishido1, Rieko Ohtsubo, Tatsumi Adachi

  • 1Pathophysiology Research Team, National Institute for Environmental Studies, Tsukuba, Japan. ishidou@nies.go.jp

Environmental Health Perspectives
|January 10, 2002
PubMed

Insights

Cadmium exposure triggers apoptosis and necrosis, but overexpressing the bcl-2 protein protects cells from these harmful effects. This suggests bcl-2 plays a key role in mitigating cadmium-induced cell death.

Area of Science:

  • Cell Biology
  • Toxicology
  • Molecular Biology

Background:

  • Cadmium is a toxic heavy metal linked to various cellular damages.
  • The bcl-2 protein family regulates apoptosis, a key process in cell death.

Purpose of the Study:

  • To investigate the impact of cadmium on bcl-2 family proteins.
  • To determine the role of bcl-2 in cadmium-induced cytotoxicity, including apoptosis and necrosis.

Main Methods:

  • Utilized cultured porcine kidney LLC-PK(1) cells and rat primary thymocytes.
  • Employed Western blot analysis to assess protein levels.
  • Investigated gene transfection for bcl-2 overexpression.
  • Performed electron microscopy to observe cellular morphology.

Main Results:

  • Cadmium exposure increased endogenous bcl-2 protein and its transcript levels in kidney cells and thymocytes.
  • Cadmium did not enhance the expression of bax, bad, or bcl-xS proteins.
  • Overexpression of bcl-2 prevented both cadmium-induced apoptosis and necrosis.
  • Lactate dehydrogenase release, a marker of necrosis, was also inhibited by bcl-2 overexpression.

Conclusions:

  • Cadmium induces apoptosis and necrosis through mechanisms that involve the bcl-2 protein.
  • Upregulation of bcl-2 protein expression can protect cells against cadmium toxicity.
  • bcl-2 plays a critical role in attenuating both apoptotic and necrotic cellular responses to cadmium.

Related Concept Videos

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...
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...
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...
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.