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Azoxystrobin induces mitochondrial dysfunction and mitochondrial pathway apoptosis by targeting the Prx1 Trp87 and

Wenjing Li1, Yajun Shen2, Lingyu Li3

  • 1Beijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing, China.

Frontiers in Pharmacology
|May 6, 2026
PubMed
Abstract

Insights

Azoxystrobin (AZOX) targets Peroxiredoxin 1 (Prx1) at specific sites, inhibiting mitochondrial function and inducing apoptosis in oral leukoplakia (OLK) cells. This mechanism offers a potential therapeutic strategy for this pre-malignant oral disorder.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Oral leukoplakia (OLK) is a significant oral potentially malignant disorder with limited therapeutic interventions.
  • Peroxiredoxin 1 (Prx1) is implicated in OLK progression, and Azoxystrobin (AZOX) has shown potential in targeting mitochondrial function.

Purpose of the Study:

  • To elucidate the precise molecular mechanism by which AZOX interacts with Peroxiredoxin 1 (Prx1) to inhibit mitochondrial function and induce apoptosis in OLK.
  • To investigate the role of specific Prx1 residues (Trp87 and Thr90) in mediating AZOX's effects.

Main Methods:

  • Molecular docking (AutoDock Vina) was used to predict AZOX-Prx1 interactions.
  • Site-directed mutagenesis was employed to create Prx1-Trp87 and Prx1-Thr90 mutants.
  • Experiments in OLK cell lines (DOK, Leuk1) assessed cell viability, apoptosis, mitochondrial ultrastructure, ROS production, membrane potential, complex III activity, energy metabolism, and protein expression.

Main Results:

  • Molecular docking identified key interactions between AZOX and Prx1 residues, including hydrogen bonds with Gln94, Thr90, Thr49, and π-π interaction with Trp87.
  • AZOX treatment significantly reduced OLK cell proliferation and induced mitochondrial apoptosis, characterized by altered Bax/Bcl-2 ratio and Cytochrome C release.
  • Mutations at Trp87 and Thr90 residues of Prx1 attenuated AZOX's inhibitory effects on mitochondrial integrity and apoptosis induction.

Conclusions:

  • AZOX exerts its anti-cancer effects by binding to Trp87 and Thr90 residues of Prx1, leading to mitochondrial dysfunction and apoptosis.
  • This interaction suppresses mitochondrial function, energy metabolism, and promotes apoptosis, offering a novel therapeutic avenue for oral leukoplakia.
Keywords:
azoxystrobinmitochondrial apoptotic pathwaymitochondrial functionoral leukoplakiaperoxiredoxin 1

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