Related Experiment Video

Updated: Jun 12, 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

Molecular events involved in ochratoxin A induced mitochondrial pathway of apoptosis, modulation by Bcl-2 family

Chayma Bouaziz1, Ossama Sharaf el dein, Cécile Martel

  • 1Laboratory of Research on Biologically Compatible Compounds, Faculty of Dentistry, Rue Avicenne, Monastir 5000, Tunisia.

Environmental Toxicology
|June 16, 2010
PubMed

Insights

Ochratoxin A (OTA) triggers apoptosis by affecting mitochondria, involving the mitochondrial permeability transition pore (PTPC) and Bcl-2 proteins. However, mitochondria are not the direct target for overcoming OTA toxicity.

Area of Science:

  • Toxicology
  • Cell Biology
  • Molecular Biology

Background:

  • Ochratoxin A (OTA) is a prevalent food-contaminating mycotoxin with known toxic effects.
  • The role of mitochondria in OTA-induced cytotoxicity requires further elucidation.

Purpose of the Study:

  • To investigate the specific role of mitochondria in ochratoxin A (OTA) cytotoxicity.
  • To determine if mitochondria are direct targets of OTA toxicity.

Main Methods:

  • Utilized human carcinoma cell lines to study OTA effects.
  • Assessed mitochondrial parameters including permeability transition pore (PTPC) opening, mitochondrial transmembrane potential (ΔΨ(m)), and reactive oxygen species (ROS) production.
  • Investigated the involvement of Bcl-2 family proteins (Bax, Bak, Bcl-2, Bcl-X(L)) in OTA-induced apoptosis.

Main Results:

  • OTA induced a mitochondria-dependent apoptotic process.
  • Key events included PTPC opening, loss of ΔΨ(m), increased O(2)(-) production, Bax relocalization, cytochrome c release, and caspase activation.
  • Purified organelle studies indicated OTA does not directly target mitochondria.
  • Mitochondrial alterations were favored by Bax and prevented by Bcl-2 and Bcl-X(L).

Conclusions:

  • Mitochondria, PTPC components, and Bcl-2 family proteins are crucial in OTA-induced apoptosis.
  • Despite their pivotal role, mitochondria are not the direct targets for overcoming OTA toxicity.

More Related Videos

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue09:27

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue

Published on: March 23, 2015

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...
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.
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...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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...