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

UV-A irradiation induces a decrease in the mitochondrial respiratory activity of human NCTC 2544 keratinocytes.

M Djavaheri-Mergny1, C Marsac, C Mazière

  • 1Laboratoire de Dermatologie, INSERM U312, Hôpital Saint-Louis, 1 rue Claude Vellefaux, 75475 Paris, France. mojgan.mergny@curie.fr

Free Radical Research
|November 8, 2001
PubMed
Summary

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

Microbial mats as model to decipher climate change effect on microbial communities through a mesocosm study.

Frontiers in microbiology·2023
Same author

Climate change influences chlorophylls and bacteriochlorophylls metabolism in hypersaline microbial mat.

The Science of the total environment·2021
Same author

Antibodies directed against annexin A2 and obstetric morbidity.

Journal of reproductive immunology·2016
Same author

Vascular expression of annexin A2 in lupus nephritis.

Journal of clinical pathology·2015
Same author

Intrafamilial heterogeneous clinical presentation of the mitochondrial 3243 MELAS mutation; molecular investigations among four generations.

European journal of neurology·2013
Same author

Antibodies against the N-terminal domain of annexin A2 in antiphospholipid syndrome.

European journal of internal medicine·2012

UV-A irradiation impairs mitochondrial respiration and ATP production in skin cells. This damage, occurring at low UV-A doses, is not caused by lipid peroxidation but activates protective systems.

Area of Science:

  • Dermatology
  • Cell Biology
  • Biochemistry

Background:

  • Ultraviolet A (UV-A) radiation is a component of sunlight known to affect skin cells.
  • Understanding the cellular mechanisms of UV-A damage is crucial for photoprotection strategies.

Purpose of the Study:

  • To investigate the impact of UV-A irradiation on mitochondrial function in human keratinocytes.
  • To determine if UV-A-induced cellular effects are mediated by lipid peroxidation.

Main Methods:

  • Human NCTC 2544 keratinocytes were exposed to UV-A radiation.
  • Cellular oxygen consumption, ATP content, and mitochondrial respiration (state 3) were measured.
  • Mitochondrial transmembrane potential and lipid peroxidation were assessed.
  • The effect of vitamin E (antioxidant) and MnSOD gene expression were analyzed.

Related Experiment Videos

Main Results:

  • UV-A exposure caused significant dose-dependent decreases in oxygen consumption and ATP content.
  • Mitochondrial respiration was inhibited, but transmembrane potential remained unaffected.
  • Vitamin E did not prevent UV-A-induced changes in respiration or ATP levels.
  • UV-A irradiation increased MnSOD gene expression, indicating enhanced mitochondrial protection.

Conclusions:

  • UV-A irradiation directly impairs mitochondrial respiratory activity in keratinocytes.
  • These mitochondrial effects occur at UV-A doses below the minimal erythemal dose.
  • The observed cellular damage is not primarily due to UV-A-induced lipid peroxidation.