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

Iron coordination by catechol derivative antioxidants

T Kawabata1, V Schepkin, N Haramaki

  • 1Department of Molecular and Cell Biology, University of California, Berkeley 94720-3200, USA.

Biochemical Pharmacology
|June 14, 1996
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

Effect of Ginkgo biloba (EGb 761) on differential gene expression.

Pharmacopsychiatry·2003
Same author

Impact of ultraviolet radiation and ozone on the transepidermal water loss as a function of skin temperature in hairless mice.

Skin pharmacology and applied skin physiology·2003
Same author

Nitric oxide synthesis and TNF-alpha secretion in RAW 264.7 macrophages: mode of action of a fermented papaya preparation.

Life sciences·2003
Same author

Morbidity risk in HFE associated hereditary hemochromatosis C282Y heterozygotes.

Toxicology·2002
Same author

High levels of diploid male production in a primitively eusocial bee (Hymenoptera: Halictidae).

Heredity·2002
Same author

Inhibition mechanisms of bioflavonoids extracted from the bark of Pinus maritima on the expression of proinflammatory cytokines.

Annals of the New York Academy of Sciences·2002

Nitrocatechol derivatives effectively inhibit iron-induced free radical reactions by sequestering iron. Iron complexes with conjugated nitrocatechols are more effective at preventing radical generation, likely due to their reduction potentials.

Area of Science:

  • Biochemistry
  • Medicinal Chemistry
  • Free Radical Chemistry

Background:

  • Iron-induced free radical reactions are implicated in various biological processes and diseases.
  • Lipid peroxidation is a key indicator of oxidative damage.
  • Catechol and nitrocatechol derivatives are known to interact with metal ions.

Purpose of the Study:

  • To synthesize iron complexes of nitrocatechol derivatives with varying substituent groups.
  • To investigate the effects of these complexes on iron-induced free radical reactions, particularly lipid peroxidation.
  • To elucidate the structure and physical properties of the iron complexes and their relationship to radical generation.

Main Methods:

  • Synthesis of iron complexes with nitrocatechol derivatives.

Related Experiment Videos

  • Investigation of iron-induced lipid peroxidation.
  • Fenton-like reaction studies to assess hydroxyl radical generation.
  • UV/vis absorption spectroscopy, Electron Spin Resonance (ESR), and 1H Nuclear Magnetic Resonance (NMR) studies.
  • Main Results:

    • Nitrocatechol derivatives effectively inhibited iron-induced lipid peroxidation.
    • Iron-catechol generated more hydroxyl radicals than iron citrate; iron-nitrocatechol derivative 2 generated a small amount, while derivatives 1 and 3 generated none.
    • Iron complexes of nitrocatechol derivatives 1 and 3 showed the highest resistance to reduction, suggesting effective iron sequestration.
    • Spectroscopic studies revealed high-spin tris(nitrocatecholato)ferrate(III) complexes in aqueous solution.

    Conclusions:

    • Nitrocatechol derivatives, especially those with conjugated structures, effectively sequester iron, preventing free radical generation.
    • The ability to keep iron in the ferric state is likely due to the reduction potentials of the nitrocatechol complexes.
    • These findings suggest potential therapeutic applications for nitrocatechol derivatives in managing iron-related oxidative stress.