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Updated: Jul 5, 2026

A Preclinical Model of Sepsis-Induced Myopathy with Disuse in Mice

A Preclinical Model of Sepsis-Induced Myopathy with Disuse in Mice

Published on: June 14, 2024

Sepsis induces brain mitochondrial dysfunction.

Joana da Costa P d'Avila¹, Ana Paula S A Santiago, Rodrigo T Amâncio

¹Laboratório de Bioquímica Redox, Programa de Biologia Molecular e Biotecnologia, Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Cidade Universitária, Rio de Janeiro, Brazil.

Critical Care Medicine

|May 23, 2008

Summary

This summary is machine-generated.

Sepsis impairs brain mitochondrial function by uncoupling oxidative phosphorylation, reducing energy production efficiency. This study reveals critical mitochondrial damage in the brain during sepsis.

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Last Updated: Jul 5, 2026

A Preclinical Model of Sepsis-Induced Myopathy with Disuse in Mice

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Published on: June 14, 2024

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Analysis of Brain Mitochondria Using Serial Block-Face Scanning Electron Microscopy

Analysis of Brain Mitochondria Using Serial Block-Face Scanning Electron Microscopy

Published on: July 9, 2016

Area of Science:

Biochemistry
Neuroscience
Pathophysiology

Background:

Mitochondrial dysfunction is implicated in sepsis pathogenesis.
A detailed examination of brain mitochondrial function during sepsis is needed.

Purpose of the Study:

To investigate brain mitochondrial function in a mouse model of sepsis.

Main Methods:

Male Swiss mice underwent cecal ligation and perforation (sepsis) or sham operation (control).
Brain mitochondrial oxygen consumption, respiratory control, membrane potential, cytochrome content, and enzyme activity were measured.

Main Results:

Sepsis increased basal oxygen consumption (state 4) and proton leak, decreasing oxidative phosphorylation efficiency.
Cytochrome content and cytochrome c oxidase activity were reduced in septic mouse brains.
Mitochondrial membrane potential recovery was impaired, and hydrogen peroxide generation was unresponsive in septic brains.

Conclusions:

Sepsis causes uncoupling of oxidative phosphorylation in the brain.
This uncoupling compromises brain tissue bioenergetic efficiency during sepsis.