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Mitochondrial dysfunction induced by leflunomide and its active metabolite.

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Leflunomide and its metabolite teriflunomide may cause liver injury by impairing mitochondrial function. This study found these drugs disrupt ATP production and mitochondrial complex V, suggesting a mechanism for drug-induced hepatotoxicity.

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ANTATP synthaseDrug-induced liver injuryLeflunomideOxidative phosphorylation

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Area of Science:

  • Pharmacology
  • Hepatotoxicity
  • Mitochondrial Biology

Background:

  • Leflunomide and teriflunomide carry black box warnings for liver injury.
  • The mechanism of drug-induced liver injury remains unclear.

Purpose of the Study:

  • To investigate the mechanism of leflunomide and A771726-induced liver injury.
  • To assess the impact of these drugs on cellular energy metabolism and mitochondrial function.

Main Methods:

  • Cytotoxicity assays using HepG2 cells.
  • Measurement of ATP levels and lactate dehydrogenase (LDH) release.
  • Analysis of mitochondrial oxidative phosphorylation (OXPHOS) complex activities.
  • Transcriptome analysis.

Main Results:

  • Leflunomide and A771726 caused time- and concentration-dependent ATP depletion and LDH release.
  • Galactose substitution exacerbated leflunomide-induced ATP decline, indicating mitochondrial liability.
  • Both drugs inhibited mitochondrial complex V (ATP synthase).
  • Bongkrekic acid attenuated drug-induced mitochondrial dysfunction and cell damage.
  • Leflunomide caused more significant transcriptomic alterations than A771726.

Conclusions:

  • Mitochondrial dysfunction is implicated in leflunomide and A771726 hepatotoxicity.
  • Leflunomide exhibits higher toxicity potency than its metabolite A771726.
  • Targeting mitochondrial complex V is a potential mechanism for drug-induced liver injury.