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

Decrease in the fluidity of brush-border membrane vesicles induced by gentamicin. A spin-labeling study.

T Moriyama1, H Nakahama, Y Fukuhara

  • 1First Department of Medicine, Osaka University Medical School, Japan.

Biochemical Pharmacology
|April 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

Enhanced Superconducting Gap in the Outer CuO_{2} Plane of the Trilayer Cuprate (Hg, Re)Ba_{2}Ca_{2}Cu_{3}O_{8+δ}.

Physical review letters·2025
Same author

Magnon interactions in a moderately correlated Mott insulator.

Nature communications·2024
Same author

Fate of charge order in overdoped La-based cuprates.

npj quantum materials·2024
Same author

Resonant photoemission spectroscopy of atomic layer Fe<sub>2</sub>N on Cu(111) with continuous angular rotation of linearly polarized light.

Journal of physics. Condensed matter : an Institute of Physics journal·2023
Same author

Evidence for a Square-Square Vortex Lattice Transition in a High-T_{c} Cuprate Superconductor.

Physical review letters·2022
Same author

Uniaxial pressure induced stripe order rotation in La<sub>1.88</sub>Sr<sub>0.12</sub>CuO<sub>4</sub>.

Nature communications·2022
Same journal

Dysregulation of the bile acid signaling network in non-alcoholic fatty liver disease: Mechanisms and a new paradigm of precision network pharmacology.

Biochemical pharmacology·2026
Same journal

hIMB1636-LDM, a novel anti-TROP2 ADC, exerts potent antitumor efficacy in pancreatic cancer via direct cytotoxicity and immune activation.

Biochemical pharmacology·2026
Same journal

CD55 glycosylation promotes ferroptotic stress tolerance in CD55-high triple-negative breast cancer.

Biochemical pharmacology·2026
Same journal

The role of Piezo1 in skeletal muscle physiology and pathology: from mechanosensing to precision therapy.

Biochemical pharmacology·2026
Same journal

Notch signaling in anti-VEGF resistant arteriolar choroidal neovascularization.

Biochemical pharmacology·2026
Same journal

Methylated SNHG3 lncRNA counteracts PSMD4-inhibited angiogenesis by HnRNPA2B1 SUMOylation in peripheral arterial disease.

Biochemical pharmacology·2026
See all related articles

Gentamicin reduces kidney membrane fluidity, inhibiting glucose transport. This effect is reversible and localized to the membrane surface, suggesting a specific binding interaction.

Area of Science:

  • Nephrology
  • Biochemistry
  • Membrane Biophysics

Background:

  • Previous work showed gentamicin decreases Na+-dependent D-glucose transport Vmax in rabbit renal brush-border membranes.
  • Gentamicin is an aminoglycoside antibiotic known for nephrotoxicity.

Purpose of the Study:

  • To investigate gentamicin's effects on the physical state of renal brush-border membranes.
  • To compare gentamicin's toxicity in outer cortex and outer medulla brush-border membranes.
  • To elucidate the mechanism of gentamicin-induced inhibition of D-glucose transport.

Main Methods:

  • Electron spin resonance (ESR) spectrometry using spin-labeled brush-border membrane vesicles.
  • Preparation of vesicles from outer cortex and outer medulla.
  • Assessment of membrane fluidity and D-glucose transport.

Related Experiment Videos

  • Recovery experiments involving washing treated membranes.

    • Main Results:

    • Gentamicin (5 mM) significantly decreased brush-border membrane fluidity.
    • Membrane fluidity was affected in outer cortical membranes at 25°C and 35°C, and outer medullary membranes only at 35°C.
    • Gentamicin's effect on fluidity was localized to the superficial membrane region.
    • Inhibition of D-glucose transport and reduced membrane fluidity were reversible upon washing.

    Conclusions:

    • Gentamicin impairs renal brush-border membrane fluidity, particularly in the superficial region.
    • This biophysical change is linked to the inhibition of Na+-dependent D-glucose transport.
    • The observed effects are reversible, suggesting a binding interaction rather than irreversible damage.