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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...
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,...
Hypoxia01:23

Hypoxia

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There are four primary types of hypoxia, each resulting from a different cause:
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Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Peroxisomes01:24

Peroxisomes

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Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Related Experiment Video

Updated: Jun 20, 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

Mitochondrial reactive oxygen species regulate hypoxic signaling.

Robert B Hamanaka1, Navdeep S Chandel

  • 1Department of Medicine, Division of Pulmonary and Critical Care Medicine, Northwestern University Medical School, Chicago, IL 60611, USA.

Current Opinion in Cell Biology
|September 29, 2009
PubMed
Summary

Physiological hypoxia triggers cellular responses via mitochondrial reactive oxygen species (ROS). Further investigation is needed to understand ROS

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A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
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A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

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Last Updated: Jun 20, 2026

Oxygen-Independent Assays to Measure Mitochondrial Function in Mammals
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A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

Area of Science:

  • Physiology
  • Cellular Biology
  • Biochemistry

Background:

  • Hypoxia elicits physiological and cellular adaptations, including altered ventilation, pulmonary artery constriction, and transcriptional changes promoting glycolysis, angiogenesis, and erythropoiesis.
  • Mitochondria, as key oxygen consumers, are implicated as cellular oxygen sensors.
  • Mitochondrial complex III produces reactive oxygen species (ROS), which mediate many hypoxia-induced cellular responses.

Purpose of the Study:

  • To provide an overview of the current understanding of mitochondrial ROS in cellular oxygen signaling during hypoxia.
  • To highlight the importance of investigating ROS as signaling molecules in maintaining cellular oxygen supply.

Main Methods:

  • Literature review of existing research on hypoxia, mitochondria, and ROS.
  • Synthesis of current knowledge regarding the role of mitochondrial-derived ROS in hypoxia signaling pathways.

Main Results:

  • Mitochondrial ROS production, particularly at complex III, is a key mediator of cellular responses to hypoxia.
  • While the precise mechanism of cytosolic ROS increase during hypoxia remains unclear, ROS function as critical signaling molecules.

Conclusions:

  • Mitochondrial-derived ROS play a significant role in cellular oxygen sensing and signaling.
  • Further research into the mechanisms and implications of ROS in hypoxia is crucial for understanding cellular oxygen homeostasis.