Chemical induction of hepatic apoptosis in rodents

Nidal A Qinna1, Bayan Y Ghanim1

  • 1University of Petra Pharmaceutical Center (UPPC), Faculty of Pharmacy and Medical Sciences, University of Petra, Amman, Jordan.

Insights

Identifying new ways to prevent liver injury is crucial. This review examines how various chemicals induce liver damage in rodents, focusing on apoptosis and other cell death types.

Area of Science:

  • Toxicology
  • Hepatology
  • Pharmacology

Background:

  • Hepatocyte injury and cell death are central to liver disease pathology.
  • Understanding cell death mechanisms, including apoptosis, is vital for developing interventions.
  • Existing research on chemical-induced cell death has led to confusion regarding multiple cell death pathways.

Purpose of the Study:

  • To review chemicals and hepatotoxicants that induce liver damage in rodents via apoptosis.
  • To explore the involvement of other cell death modes like necrosis and fibrosis.
  • To analyze the mechanisms of hepatotoxicity initiation in rodent hepatocytes.

Main Methods:

  • Review of scientific literature on chemical-induced liver injury in rodents.
  • Analysis of studies detailing apoptosis and other cell death pathways.
  • Examination of various chemical classes: hepatotoxins, mycotoxins, hyperglycemia inducers, metallic nanoparticles, and immunosuppressants.

Main Results:

  • Several chemicals and potential hepatotoxicants induce liver damage in rodents primarily through apoptosis.
  • Evidence suggests the involvement of other cell death modalities, complicating the precise understanding of injury.
  • Different rodent models exhibit varied responses to hepatotoxic agents, impacting research outcomes.

Conclusions:

  • Chemicals can induce liver injury in rodents through apoptosis, but other cell death mechanisms may also contribute.
  • A comprehensive understanding of diverse cell death pathways is necessary for effective liver disease treatment development.
  • Selecting appropriate rodent models is critical for accurate research on hepatotoxicity and potential interventions.

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