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Ritonavir-induced hepatotoxicity and ultrastructural changes of hepatocytes

Chang-Chun Kuang1, Ying Wang, Peng-Chao Hu

  • 1Department of Pathology and Pathophysiology, Hubei Provincial Key Laboratory of Developmentally Originated Disease, School of Medicine, Wuhan University , Wuhan, Hubei , PR China and.

Ultrastructural Pathology
|August 1, 2014
PubMed

Insights

Ritonavir (RTV) inhibits liver cell proliferation by inducing apoptosis. This study observed cellular changes and increased cleaved caspase-3, indicating RTV

Area of Science:

  • Hepatology
  • Toxicology
  • Molecular Biology

Background:

  • Ritonavir (RTV) is an antiretroviral medication.
  • Hepatotoxicity is a known concern with RTV treatment.
  • The precise mechanism of RTV-induced liver injury requires further elucidation.

Purpose of the Study:

  • To investigate the effects of ritonavir on hepatocyte proliferation.
  • To determine the role of apoptosis in ritonavir-induced hepatotoxicity.
  • To identify cellular and ultrastructural changes in hepatocytes following ritonavir exposure.

Main Methods:

  • Detection of cleaved caspase-3 expression levels in hepatocytes.
  • Morphological and ultrastructural examination of hepatocytes from RTV-treated mice using electron microscopy.

Main Results:

  • Ritonavir significantly inhibited hepatocyte proliferation.
  • Cleaved caspase-3 expression levels were increased in RTV-treated hepatocytes.
  • Electron microscopy revealed characteristic apoptotic changes: chromatin margination, mitochondrial damage, karyopyknosis, and cytoplasmic vacuolization.

Conclusions:

  • Ritonavir induces apoptosis in hepatocytes.
  • The caspase-cascade system is implicated in ritonavir's hepatotoxic mechanism.
  • Understanding these mechanisms can inform strategies to mitigate RTV-associated liver injury.
Keywords:
Apoptosishepatotoxicityritonavirultrastructure

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