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Electron Transport Chain: Complex I and II

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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.
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Updated: May 13, 2026

An Improved Method to Isolate Mitochondrial Contact Sites

An Improved Method to Isolate Mitochondrial Contact Sites

Published on: June 16, 2023

Mitochondrial complex I.

¹Medical Research Council Mitochondrial Biology Unit, Cambridge, CB2 0XY, United Kingdom. jh@mrc-mbu.cam.ac.uk

Annual Review of Biochemistry

|March 27, 2013

Summary

Complex I is vital for cellular respiration and energy production. This review examines its mechanisms, focusing on energy transduction, superoxide production, and links to human diseases.

Area of Science:

Biochemistry
Cellular Respiration
Mitochondrial Function

Background:

Complex I (NADH:ubiquinone oxidoreductase) is essential for aerobic respiration in mitochondria.
It oxidizes NADH, reduces ubiquinone, and translocates protons, contributing to the proton-motive force.
Complex I is a significant source of cellular reactive oxygen species.

Purpose of the Study:

To review current data on energy transduction mechanisms in Complex I.
To discuss models of superoxide production by Complex I.
To explore the role of Complex I dysfunction in human diseases.

Main Methods:

Literature review of extant data.
Evaluation of contemporary mechanistic models.
Analysis of studies on Complex I function and dysfunction.

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An Improved Method to Isolate Mitochondrial Contact Sites

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Isolation of Mitochondria for Mitochondrial Supercomplex Analysis from Small Tissue and Cell Culture Samples

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Main Results:

The redox reactions occur in the hydrophilic domain, involving NADH oxidation, electron transfer via iron-sulfur clusters, and ubiquinone reduction.
Proton translocation in the membrane domain requires long-range energy transfer, with coupling mechanisms currently unknown.
Complex I is implicated in various human diseases due to its dysfunction.

Conclusions:

Understanding the mechanisms of energy transduction and superoxide production is crucial.
Further mechanistic studies are needed to elucidate the coupling of redox and proton-transfer reactions.
Investigating Complex I dysfunctions offers insights into human disease pathogenesis.