Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Electron Transport Chain: Complex I and II

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 Membranes

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,...

Mitochondria

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

First molecular detection of <i>Theileria haneyi</i> infection in horses in Southern Spain.

Frontiers in veterinary science·2026

Same author

Impact of timely vaccination and genomic surveillance on controlling consecutive waves of SARS-CoV-2 variants.

Scientific reports·2026

Same author

Neuroprotective Role of Cannabinoid CB<sub>1</sub> and GPR55 Receptors in a Cell Model of Multiple Sclerosis.

Molecular neurobiology·2026

Same author

Discrete interneuron subsets participate in GluN1/GluN3A excitatory glycine receptor (eGlyR)-mediated regulation of hippocampal network activity throughout development and evolution.

Research square·2025

Same author

Apolipoprotein D Expression Dynamics During Cuprizone-Induced Demyelination and Remyelination in a Mouse Model of Multiple Sclerosis.

International journal of molecular sciences·2025

Same author

True Prevalence and Seroprevalence of Piroplasmosis in Horses in Southwestern Europe.

Animals : an open access journal from MDPI·2025

Search research articles

Related Experiment Video

Updated: Jul 18, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

Mitochondrial dysfunction in human colorectal cancer progression.

Maria-Jesus Sanchez-Pino¹, Pilar Moreno, Ana Navarro

¹Department of Biochemistry and Molecular Biology, School of Medicine, University of Cadiz, Spain. mariajesus.sanchez@uca.es

Frontiers in Bioscience : a Journal and Virtual Library

|November 28, 2006

Summary

Mitochondria in human colorectal cancer exhibit increased oxidative damage and altered activity, impacting cellular signaling. This damage and nitric oxide diffusion may promote cancer progression and cell death in surrounding tissues.

More Related Videos

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

Analytical Determination of Mitochondrial Function of Excised Solid Tumor Homogenates

Analytical Determination of Mitochondrial Function of Excised Solid Tumor Homogenates

Published on: August 6, 2021

Related Experiment Videos

Last Updated: Jul 18, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

Analytical Determination of Mitochondrial Function of Excised Solid Tumor Homogenates

Analytical Determination of Mitochondrial Function of Excised Solid Tumor Homogenates

Published on: August 6, 2021

Area of Science:

Biochemistry
Cell Biology
Oncology

Background:

Mitochondria play a crucial role in cellular signaling, with dysfunction linked to cancer.
Mitochondrial oxidative damage, nitric oxide (NO), and hydrogen peroxide (H2O2) diffusion are implicated in colorectal cancer progression.

Purpose of the Study:

To investigate mitochondrial dysfunction and oxidative stress in human colorectal tumors and adjacent non-tumor tissues.
To explore the role of mitochondrial-derived signaling molecules in cancer progression.

Main Methods:

Analysis of oxidative damage markers (TBARS, protein carbonyls) in mitochondria.
Measurement of mitochondrial enzyme activities (NADH-cytochrome c reductase, cytochrome oxidase).
Assessment of superoxide dismutase (SOD) and mitochondrial nitric oxide synthase (mtNOS) activities.

Main Results:

Significantly increased oxidative damage (TBARS, protein carbonyls) in tumor and adjacent non-tumor mitochondria, with protein carbonyls being a sensitive indicator.
Decreased mitochondrial enzyme activities (NADH-cytochrome c reductase, cytochrome oxidase) in both tumor and adjacent tissues.
Increased mtNOS activity in advanced-stage tumors and adjacent tissues, correlating with oxidative damage.

Conclusions:

Mitochondrial dysfunction and oxidative stress are present in both colorectal tumors and surrounding non-tumor tissues.
Mitochondrial-derived NO and H2O2 may signal for cell death in adjacent tissues, acting as toxohormones and contributing to cancer progression.