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Related Experiment Video

Updated: May 9, 2026

Simultaneous Measurement of Superoxide/Hydrogen Peroxide and NADH Production by Flavin-containing Mitochondrial Dehydrogenases

Simultaneous Measurement of Superoxide/Hydrogen Peroxide and NADH Production by Flavin-containing Mitochondrial Dehydrogenases

Published on: February 24, 2018

Mitochondrial dysfunction indirectly elevates ROS production by the endoplasmic reticulum.

Michael P Murphy¹

¹MRC Mitochondrial Biology Unit, Cambridge, UK. mpm@mrc-mbu.cam.ac.uk

Cell Metabolism

|August 13, 2013

Summary

This summary is machine-generated.

Damaged mitochondria signal to the endoplasmic reticulum, increasing reactive oxygen species (ROS) production. This study reveals a complex link between mitochondrial damage and ROS, extending beyond the organelle itself.

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Area of Science:

Cell biology
Mitochondrial research
Reactive oxygen species

Background:

Mitochondrial dysfunction is commonly linked to elevated reactive oxygen species (ROS) production within the mitochondria.
The precise relationship between mitochondrial damage and cellular ROS levels is not fully understood.

Purpose of the Study:

To investigate the complex interplay between mitochondrial damage and ROS production.
To determine if signals from damaged mitochondria influence ROS production in other cellular compartments.

Main Methods:

Utilized yeast as a model organism.
Investigated signaling pathways originating from damaged mitochondria.
Measured ROS production at the endoplasmic reticulum surface.

Main Results:

Demonstrated that signals from damaged mitochondria can indeed increase ROS production.
Identified the endoplasmic reticulum as a site of increased ROS generation in response to mitochondrial damage.
Revealed a more intricate connection between mitochondrial health and cellular oxidative stress than previously assumed.

Conclusions:

The link between mitochondrial damage and ROS production is more complex than a direct organelle-specific effect.
Signaling from damaged mitochondria impacts ROS production at the endoplasmic reticulum, suggesting broader cellular communication.
Findings in yeast highlight novel mechanisms of cellular response to mitochondrial dysfunction.