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Protection from amphotericin B-induced lipid peroxidation in rats by fructose-1,6-diphosphate

M R Rao1, K D Olinde, A K Markov

  • 1Department of Medicine, University of Mississippi Medical Center, Jackson 39216, USA.

Research Communications in Molecular Pathology and Pharmacology
|February 1, 1997
PubMed

Insights

Amphotericin B causes toxic side effects by increasing lipid peroxide damage in rat organs. Fructose-1,6-diphosphate (FDP) pretreatment partially protected against this Amphotericin B toxicity.

Area of Science:

  • Pharmacology
  • Toxicology
  • Biochemistry

Background:

  • Amphotericin B (Amp B) is a vital antifungal medication.
  • Amp B treatment is limited by significant cellular toxicity.
  • Lipid peroxidation is a known mechanism of cellular damage.

Purpose of the Study:

  • To investigate the in vivo effects of Amp B on lipid peroxide levels in rat organs.
  • To determine the protective potential of fructose-1,6-diphosphate (FDP) against Amp B-induced toxicity.

Main Methods:

  • Rats were administered a lethal dose of Amp B (1.5 mg/kg).
  • Malondialdehyde (MDA) levels, a marker of lipid peroxidation, were measured in kidney, brain, liver, lung, and heart.
  • Rats were pretreated with FDP (0.35 g/kg) before Amp B infusion in a separate group.

Main Results:

  • Amp B infusion led to cardiac arrest in rats.
  • Kidney tissues showed the highest increase in MDA levels, followed by brain, liver, lung, and heart.
  • FDP pretreatment significantly reduced MDA formation across all measured organs.

Conclusions:

  • Amp B-induced toxicity in rats is associated with increased lipid peroxidation.
  • FDP demonstrates partial protective effects against Amp B toxicity by mitigating lipid peroxide damage.

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