Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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...

You might also read

Related Articles

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

Sort by
Same author

Evaluating the Informed Consent Objective Structured Clinical Exam (OSCE) Using a Minimum Standard Assessment Tool During the Transition-to-Residency Program.

Cureus·2026
Same author

Elevated mitochondrial protein import in acute myeloid leukemia increases reliance on mitochondrial protease LONP1.

The Journal of clinical investigation·2026
Same author

Mitochondrial RNA degradation regulates differentiation, stemness, and immune sensitivity in acute myeloid leukemia.

Nature communications·2026
Same author

Critical Illness Outcomes of Hospitalized Pregnant Women Following a Texas Abortion Ban.

American journal of respiratory and critical care medicine·2026
Same author

Climate Change and Extreme Weather Event Adaptations for Individuals With Dementia: A Systematic Review.

Brain and behavior·2026
Same author

Glycemic Control and Utilization Risk With the Conversion of Glimepiride to Glipizide in Adults 64 Years and Older at an Integrated Health Care System.

Journal of the American Geriatrics Society·2026

Related Experiment Video

Updated: Jul 10, 2026

Induction of Mouse Lung Injury by Endotracheal Injection of Bleomycin
06:52

Induction of Mouse Lung Injury by Endotracheal Injection of Bleomycin

Published on: April 30, 2019

18.9K

Mitochondrial DNA damage by bleomycin induces AML cell death.

ManTek Yeung1, Rose Hurren, Carine Nemr

  • 1Princess Margaret Cancer Centre, Ontario Cancer Institute, University Health Network, Room 7-116, 610 University Ave, Toronto, ON, M5G 2M9, Canada.

Apoptosis : an International Journal on Programmed Cell Death
|March 31, 2015
PubMed
Summary

Bleomycin damages mitochondrial DNA (mtDNA) in acute myeloid leukemia (AML) cells, impairing mitochondrial function and leading to cell death. This suggests mtDNA-targeted therapies, like bleomycin, may effectively treat AML.

More Related Videos

An Automated Differential Nuclear Staining Assay for Accurate Determination of Mitocan Cytotoxicity
07:58

An Automated Differential Nuclear Staining Assay for Accurate Determination of Mitocan Cytotoxicity

Published on: May 12, 2020

7.6K
Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
06:03

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Published on: May 9, 2025

2.3K

Related Experiment Videos

Last Updated: Jul 10, 2026

Induction of Mouse Lung Injury by Endotracheal Injection of Bleomycin
06:52

Induction of Mouse Lung Injury by Endotracheal Injection of Bleomycin

Published on: April 30, 2019

18.9K
An Automated Differential Nuclear Staining Assay for Accurate Determination of Mitocan Cytotoxicity
07:58

An Automated Differential Nuclear Staining Assay for Accurate Determination of Mitocan Cytotoxicity

Published on: May 12, 2020

7.6K
Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
06:03

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Published on: May 9, 2025

2.3K

Area of Science:

  • Mitochondrial biology
  • Cancer therapeutics
  • Hematologic malignancies

Background:

  • Mitochondria possess their own genome (mtDNA), crucial for cellular function.
  • Mitochondrial dysfunction is implicated in various diseases, including cancer.
  • Targeting cancer cell-specific vulnerabilities is a key therapeutic strategy.

Purpose of the Study:

  • To investigate the impact of mitochondrial DNA (mtDNA) damage on acute myeloid leukemia (AML) cell function and viability.
  • To identify chemotherapeutic agents capable of damaging mtDNA in AML cells.
  • To evaluate bleomycin as a potential mtDNA-targeted therapy for AML.

Main Methods:

  • Screening of DNA-damaging chemotherapeutic agents for mtDNA damage in AML cells.
  • Assessment of mitochondrial mass and oxygen consumption following bleomycin treatment.
  • Evaluation of bleomycin's efficacy in AML xenograft mouse models.
  • Comparative analysis of bleomycin-induced mtDNA damage in AML cells versus normal lung tissue.

Main Results:

  • Bleomycin was identified as an agent that damages mtDNA in AML cells at cytotoxic concentrations.
  • Bleomycin treatment reduced mitochondrial mass and basal oxygen consumption in AML cells.
  • mtDNA damage was functionally critical for bleomycin-induced AML cell death.
  • Bleomycin demonstrated preferential mtDNA damage in AML cells over normal lung tissue and delayed tumor growth in vivo.

Conclusions:

  • Mitochondrial DNA-targeted therapy represents a promising strategy for AML treatment.
  • Bleomycin exhibits selective toxicity towards AML cells via mtDNA damage, suggesting its potential clinical utility.
  • Further investigation into bleomycin's role in AML therapy is warranted.