Related Experiment Video

Updated: Jun 22, 2026

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
09:44

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

Characterization of ochratoxin A-induced apoptosis in primary rat hepatocytes

Martin Chopra1, Pascal Link, Christine Michels

  • 1Institute of Food Chemistry and Toxicology, University of Kaiserslautern, Erwin Schrödinger Strasse 52, 67659 Kaiserslautern, Germany.

Cell Biology and Toxicology
|June 30, 2009
PubMed

Insights

Ochratoxin A (OTA) induces programmed cell death (apoptosis) in rat liver cells, affecting DNA damage and cell signaling pathways. While caspases are involved, other mechanisms also contribute to OTA-induced liver cell death.

Area of Science:

  • Hepatology
  • Toxicology
  • Molecular Biology

Background:

  • Ochratoxin A (OTA) is a mycotoxin primarily targeting kidneys but also exhibiting hepatotoxicity.
  • OTA exposure can disrupt cellular signaling and induce apoptosis even at low concentrations.
  • Previous studies focused on OTA's effects on kidney cells, necessitating research into its impact on liver cells.

Purpose of the Study:

  • To investigate apoptosis-related events induced by OTA in primary rat hepatocytes.
  • To analyze changes in gene expression associated with apoptosis following OTA treatment.
  • To elucidate the mechanisms underlying OTA-induced hepatocyte apoptosis.

Main Methods:

  • Primary rat hepatocytes were treated with 1 microM OTA for 24 hours.
  • Pathway-specific polymerase chain reaction arrays were used to assess apoptosis-related gene expression.
  • Protein biosynthesis inhibition, mitochondrial apoptosis-inducing factor release, caspase activity, and chromatin changes were evaluated.

Main Results:

  • OTA treatment upregulated key apoptosis-related genes, including apaf1, bad, caspase 7, DNA polymerase beta (polb), and p53.
  • FAS and faslg were significantly induced, indicating involvement of the extrinsic apoptosis pathway.
  • OTA caused concentration-dependent inhibition of protein biosynthesis, released apoptosis-inducing factor from mitochondria, increased caspase activity (caspases 8, 9, and 3/7), and induced chromatin condensation and fragmentation.

Conclusions:

  • Ochratoxin A induces p53-dependent apoptosis in rat hepatocytes.
  • While caspase activation plays a role, OTA-induced apoptosis involves other caspase-independent and protein biosynthesis-independent mechanisms.
  • These findings highlight the complex molecular pathways through which OTA exerts its hepatotoxic effects.

More Related Videos

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method08:04

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method

Published on: October 23, 2018

Inducing Acute Liver Injury in Rats via Carbon Tetrachloride (CCl4) Exposure Through an Orogastric Tube06:12

Inducing Acute Liver Injury in Rats via Carbon Tetrachloride (CCl4) Exposure Through an Orogastric Tube

Published on: April 28, 2020

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.