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 Experiment Videos

ATP hydrolysis by ischemic mitochondria.

J B Classen1, W J Mergner, M Costa

  • 1Department of Pathology, University of Maryland School of Medicine, Baltimore 21201.

Journal of Cellular Physiology
|October 1, 1989
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Pertussis infections, vaccines and Type 1 diabetes.

Diabetic medicine : a journal of the British Diabetic Association·2004
Same author

Clustering of cases of type 1 diabetes mellitus occurring 2-4 years after vaccination is consistent with clustering after infections and progression to type 1 diabetes mellitus in autoantibody positive individuals.

Journal of pediatric endocrinology & metabolism : JPEM·2003
Same author

Vaccines and the risk of insulin-dependent diabetes (IDDM): potential mechanism of action.

Medical hypotheses·2001
Same author

Hemophilus vaccine associated with increased risk of diabetes: causality likely.

Diabetes care·2000
Same author

Immunisation and type 1 diabetes mellitus: is there a link?

Drug safety·1999
Same author

Immunization in the first month of life may explain decline in incidence of IDDM in The Netherlands.

Autoimmunity·1999
Same journal

Mt1-Ca<sup>2+</sup>-Mitochondrial Metabolic Axis Maintains Temporomandibular Joint Condylar Cartilage Homeostasis Under Low Oxygen and Hypoxic Condition.

Journal of cellular physiology·2026
Same journal

Correction to "IRE1α/NOX4 Signaling Pathway Mediates Ros-Dependent Activation of Hepatic Stellate Cells in NaAsO<sub>2</sub>-Induced Liver Fibrosis".

Journal of cellular physiology·2026
Same journal

Lipocalin-2 Restores Mitochondrial and Antioxidant Adaptation in a Strain-Specific Manner During LPS Induced Sepsis.

Journal of cellular physiology·2026
Same journal

Dysregulation of Non-Muscle Myosin IIA Assembly and Phosphorylation in S100A4 Null Mouse Lens.

Journal of cellular physiology·2026
Same journal

Corrigendum to "A Probiotic Combination of Limosilactobacillus reuteri and Clostridium butyricum Ameliorates 5-Fluorouracil-Induced Intestinal Mucositis in Rats by Strengthening Barrier Integrity and Modulating Immuno-Microbial Homeostasis".

Journal of cellular physiology·2026
Same journal

Sexually Dimorphic Regulation of MiR-29a/c-3p in Human Endothelial Cells: Cell Functions and Transcriptome.

Journal of cellular physiology·2026
See all related articles

Cellular adenosine triphosphate (ATP) levels decrease after ischemia. This study found that reduced ATP production, not increased ATP hydrolysis, is the main cause of low ATP levels in damaged heart mitochondria.

Area of Science:

  • Biochemistry
  • Cellular Biology
  • Cardiovascular Research

Background:

  • Cellular adenosine triphosphate (ATP) levels are critical for cell function and are maintained by production and hydrolysis rates.
  • Ischemia, a condition of reduced blood flow, impairs mitochondrial function, affecting both ATP production and hydrolysis.
  • Understanding the primary cause of ATP depletion in ischemia is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate whether decreased ATP production or increased ATP hydrolysis is the primary driver of mitochondrial dysfunction during ischemia.
  • To elucidate the role of mitochondrial damage in altering ATP homeostasis following ischemic events.

Main Methods:

  • Isolated rat heart mitochondria subjected to 45 minutes of warm ischemia to induce damage.

Related Experiment Videos

  • Measurement of ATP levels using the luciferin-luciferase assay in cuvettes containing normal or ischemic mitochondria.
  • Experimental setup included mixtures of coupled and uncoupled mitochondria to simulate varying conditions.

    • Main Results:

    • Mitochondria damaged by prolonged ischemia exhibited accelerated ATP hydrolysis compared to normal mitochondria.
    • Normal mitochondria demonstrated the capacity to compensate for increased ATP hydrolysis when mixed with uncoupled mitochondria.
    • The rate of ATP hydrolysis by damaged mitochondria was not sufficient to account for the observed drastic reduction in cellular ATP levels.

    Conclusions:

    • The primary cause of significantly reduced cellular ATP levels following irreversible ischemia is diminished ATP synthesis by damaged mitochondria.
    • Increased ATP hydrolysis by ischemic mitochondria plays a secondary role in ATP depletion.
    • These findings highlight the critical impact of impaired mitochondrial ATP production on cellular energy status during ischemic injury.