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Related Concept Videos

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...
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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,...
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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...

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Updated: Jun 4, 2026

Oxygen-Independent Assays to Measure Mitochondrial Function in Mammals
05:59

Oxygen-Independent Assays to Measure Mitochondrial Function in Mammals

Published on: May 19, 2023

Do G4 ligands induce mitochondrial dysfunction without ROS induction.

Xinru Zhang1,2, Fei Li1, Siyi Zeng1

  • 1Key Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu 610041, China.

Iscience
|June 3, 2026
PubMed
Summary
This summary is machine-generated.

G-quadruplex (G4) DNA ligands target cancer cells by disrupting mitochondrial function without causing reactive oxygen species (ROS) bursts. This selective G4 targeting offers a novel anticancer strategy with reduced toxicity.

Keywords:
Biochemistrycell biologymolecular biology

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Genomics

Background:

  • G-quadruplex (G4) DNA structures are increasingly recognized as promising therapeutic targets due to their presence in nuclear and mitochondrial genomes.
  • Understanding the cellular effects of G4 ligands is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To develop and utilize a mitochondrial high-content profiling platform (Mito-HiCP) to compare the effects of G4 ligands and cisplatin on cancer and normal cells.
  • To elucidate the mechanism of action of G4 ligands, particularly their impact on mitochondrial function and reactive oxygen species (ROS) production.

Main Methods:

  • Development of the Mito-HiCP platform integrating automated microscopy and quantitative image analysis.
  • Comparative analysis of G4 ligands (including 360 A and its isomer EDL21) and cisplatin in various cell types.
  • Assessment of mitochondrial membrane potential, ROS levels, mitochondrial DNA copy number, transcription, and electron transport chain protein expression.

Main Results:

  • G4 ligands induce mitochondrial depolarization without ROS bursts, unlike cisplatin which is associated with ROS.
  • The G4 ligand 360 A selectively reduces ROS levels in both mitochondria and cytosol and demonstrates tumor selectivity.
  • 360 A's isomer (EDL21), which does not bind G4 DNA, showed no significant effect, confirming a G4-dependent mechanism.
  • Mechanistically, 360 A decreases mitochondrial DNA copy number, transcription, and electron transport chain protein levels.
  • G4 targeting was shown to uncouple mitochondrial membrane potential from ROS production.

Conclusions:

  • G4 ligands represent a distinct class of anticancer agents that target mitochondria selectively.
  • The developed Mito-HiCP platform is effective for dissecting mitochondrial responses and redox regulation.
  • G4 targeting offers a novel mode of redox regulation for selective anticancer activity, distinct from ROS-inducing chemotherapies.