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

Nitric oxide and cell death.

M P Murphy1

  • 1Department of Biochemistry, University of Otago, Box 56, Dunedin, New Zealand. murphy@sanger.otago.ac.nz

Biochimica Et Biophysica Acta
|May 13, 1999
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

Mitochondrial complex I activity in microglia sustains neuroinflammation.

Nature·2024
Same author

Mitochondrial reverse electron transport in myeloid cells perpetuates neuroinflammation.

bioRxiv : the preprint server for biology·2024
Same author

Chronic Fragmentation of the Daily Sleep-Wake Rhythm Increases Amyloid-beta Levels and Neuroinflammation in the 3xTg-AD Mouse Model of Alzheimer's Disease.

Neuroscience·2021
Same author

Mitochondria-targeted antioxidant MitoQ ameliorates ischaemia-reperfusion injury in kidney transplantation models.

The British journal of surgery·2021
Same author

Ex vivo normothermic perfusion of isolated segmental porcine bowel: a novel functional model of the small intestine.

BJS open·2021
Same author

Translatable mitochondria-targeted protection against programmed cardiovascular dysfunction.

Science advances·2020
Same journal

Cumulative Contents.

Biochimica et biophysica acta·2020
Same journal

Molecular Basis of Disease Cumulative Contents.

Biochimica et biophysica acta·2020
Same journal

General Subjects Cumulative Contents.

Biochimica et biophysica acta·2020
Same journal

Erratum to 'on the role of exchangeable hydrogen bonds for the kinetics of P680<sup>+·</sup> Q<sub>A</sub> <sup>-·</sup> formation and P680<sup>+·</sup> Pheo<sup>-·</sup> recombination in photosystem II' [Biochim. Biophys. Acta 1276 (1996) 35-44].

Biochimica et biophysica acta·2019
Same journal

Oligomeric state of the light-harvesting complexes B800-850 and B875 from purple bacterium Rubrivivax gelatinosus in detergent solution.

Biochimica et biophysica acta·2019
Same journal

Regulation of pigment content and enzyme activity in the cyanobacterium Nostoc sp. Mac grown in continuous light, a light-dark photoperiod, or darkness.

Biochimica et biophysica acta·2019
See all related articles

Unregulated nitric oxide (NO) production triggers cell death via oxidative stress and metabolic disruption. This review explores NO

Area of Science:

  • Biochemistry
  • Cell Biology
  • Toxicology

Background:

  • Nitric oxide (NO) plays vital roles in mammalian physiology.
  • Excessive NO production can induce cellular damage and death.
  • Mechanisms of NO-induced cell death are complex and context-dependent.

Purpose of the Study:

  • To review the molecular mechanisms by which nitric oxide (NO) causes cell death.
  • To discuss the contribution of NO to pathological conditions like ischemia-reperfusion injury and neurodegeneration.

Main Methods:

  • Literature review of scientific articles on nitric oxide.
  • Analysis of pathways leading to NO-induced cell death.
  • Synthesis of information on NO's role in disease.

Related Experiment Videos

Main Results:

  • Unregulated NO production leads to cell death through oxidative stress, impaired energy metabolism, DNA damage, and calcium dysregulation.
  • NO-induced cell death can manifest as apoptosis or necrosis.
  • NO is implicated in the pathogenesis of ischemia-reperfusion injury and neurodegenerative diseases.

Conclusions:

  • Nitric oxide mediates cell death through diverse biochemical pathways.
  • Understanding NO's cytotoxic mechanisms is crucial for developing therapies for ischemia-reperfusion injury and neurodegeneration.