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Related Concept Videos

Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
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...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
The Electron Transport Chain01:30

The Electron Transport Chain

The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q in...
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...
ATP Synthase: Mechanism01:48

ATP Synthase: Mechanism

In animals, the mitochondrial F1F0 ATP synthase is the key protein that synthesizes ATP molecules through a complex catalytic mechanism. While the nuclear genome encodes the majority of ATP synthase subunits, the mitochondrial genome encodes some of the enzyme's most critical components. The formation of this multi-subunit enzyme is a complex multi-step process regulated at the level of transcription, translation, and assembly. Defects in one or more of these steps can result in decreased ATP...

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Updated: May 13, 2026

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models
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Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models

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Hepatitis C virus-induced mitochondrial dysfunctions.

Charlène Brault1, Pierre L Levy, Birke Bartosch

  • 1CRCL, INSERM U1052, CNRS 5286, Université de Lyon, 151, Cours A Thomas 69424 Lyon Cedex, France. charlene.brault@inserm.fr

Viruses
|March 23, 2013
PubMed
Summary

Hepatitis C virus (HCV) infection causes liver metabolic disorders and oxidative stress, potentially leading to cancer. Mitochondrial dysfunction is implicated, but its precise role requires further investigation in relevant models.

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Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides

Published on: September 16, 2020

Area of Science:

  • Hepatology and Virology
  • Mitochondrial Biology
  • Oncogenesis

Background:

  • Chronic hepatitis C is associated with liver metabolic dysfunction, oxidative stress, inflammation, and regeneration, contributing to hepatocellular carcinoma.
  • Mitochondrial dysfunctions, affecting metabolism, oxidative stress, calcium signaling, and apoptosis, are central to these pathological processes.
  • Hepatitis C virus (HCV) proteins interacting with mitochondria are suggested, but their precise impact on mitochondrial function remains unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which HCV induces mitochondrial dysfunctions.
  • To determine the role of these mitochondrial dysfunctions in viral replication and liver disease progression, including neoplastic transformation.
  • To address inconsistencies in current research by investigating these aspects in physiologically relevant model systems.

Main Methods:

  • Review and synthesis of existing in vitro and in vivo studies on HCV-mitochondria interactions.
  • Emphasis on the need for studies using productively replicating virus in physiologically relevant cell and animal models.
  • Focus on molecular aspects of mitochondrial dysfunction and its pathological consequences.

Main Results:

  • Evidence suggests HCV proteins localize to mitochondria, but functional consequences are contradictory, likely due to artificial experimental systems.
  • In vivo studies are complicated by superimposed immune responses, obscuring direct viral effects on mitochondria.
  • The exact contribution of HCV-induced mitochondrial dysfunctions to disease progression and cancer development remains undetermined.

Conclusions:

  • Clarifying HCV's direct impact on mitochondrial function requires advanced, physiologically relevant models.
  • Understanding these molecular mechanisms is crucial for deciphering HCV pathogenesis and developing targeted therapies.
  • Further research is needed to confirm the role of mitochondrial dysfunctions in viral replication and hepatocellular carcinoma development.