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Gentamicin aggravates renal injury by affecting mitochondrial dynamics, altering renal transporters expression, and

Mingkang Zhang1, Yan Zhou2, Xiujuan Wang1

  • 1Department of Pharmacy, The First Hospital of Lanzhou University, Lanzhou, Gansu 730000, China; School of Pharmacy, Lanzhou University, Lanzhou, Gansu 730000, China.

Toxicology Letters
|July 28, 2025
PubMed

Insights

Gentamicin antibiotic damages kidney cells by impairing mitochondria and promoting apoptosis. Early detection of this drug-induced kidney injury remains a challenge.

Area of Science:

  • Nephrology
  • Toxicology
  • Mitochondrial Biology

Background:

  • Drug-induced nephrotoxicity is a major cause of hospital-acquired acute kidney injury (AKI).
  • Gentamicin, an aminoglycoside antibiotic, is frequently used but limited by kidney toxicity.
  • Mitochondrial dysfunction is a key factor in AKI, making it a therapeutic target.

Purpose of the Study:

  • To investigate the mechanisms of gentamicin-induced nephrotoxicity.
  • To elucidate the role of mitochondrial dysfunction in gentamicin's kidney damage.
  • To explore potential therapeutic strategies for AKI.

Main Methods:

  • In vitro experiments using renal tubular epithelial cells.
  • Dose- and time-dependent exposure to gentamicin.
  • Assessment of mitochondrial structure, membrane potential, and reactive oxygen species (ROS).
  • Analysis of renal transporters, mitochondrial dynamics proteins (OPA1, Mitofusin1/2, DRP1), and apoptosis markers (Bax/Bcl2-Caspase3 pathway).

Main Results:

  • Gentamicin induced dose- and time-dependent damage to renal tubular epithelial cells.
  • Observed were impaired mitochondrial structure, decreased membrane potential, and increased ROS.
  • Gentamicin altered renal transporters, disrupted mitochondrial dynamics, and promoted apoptosis.
  • Standard biomarkers like serum creatinine and blood urea nitrogen (BUN) did not accurately detect early gentamicin-induced kidney injury.

Conclusions:

  • Gentamicin causes nephrotoxicity through mitochondrial dysfunction and apoptosis induction.
  • Current biomarkers are insufficient for early detection of gentamicin-induced kidney injury.
  • Understanding these mechanisms provides a basis for managing gentamicin's clinical use and developing AKI therapies.
Keywords:
ApoptosisGentamicinMitochondriaRenal injuryTransporters

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