ArticleFrontiers in pharmacology2026
Azoxystrobin induces mitochondrial dysfunction and mitochondrial pathway apoptosis by targeting the Prx1 Trp87 and Thr90 sites in oral leukoplakia.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Oral leukoplakia (OLK) is a prevalent oral potentially malignant disorder with limited treatment options. Our previous research showed that Azoxystrobin (AZOX) induces apoptosis and inhibits mitochondrial complex III activity. Peroxiredoxin 1 (Prx1) plays an important role in OLK progression, and preliminary evidence suggests AZOX may target Prx1 to disrupt mitochondrial function. This study aims to elucidate the precise molecular mechanism by investigating AZOX's interaction with specific Prx1 residues. Methods: We employed AutoDock Vina for molecular docking to predict AZOX-Prx1 interactions. Using seamless cloning, Prx1-WT, Prx1-Trp87 mutant, and Prx1-Thr90 mutant variants were constructed and expressed in DOK and Leuk1 OLK cell lines. Comprehensive assessments included cell viability (Cell Counting Kit-8, CCK-8), apoptosis (flow cytometry), mitochondrial ultrastructure (transmission electron microscopy, TEM), mitochondrial ROS (mtROS) production, membrane potential (MMP), complex III activity, cellular energy metabolism (mitochondrial stress assay), and expression of mitochondrial apoptosis-related proteins (Western blot/immunofluorescence). Results: Molecular docking revealed AZOX forms four hydrogen bonds with the Gln94, Thr90, and Thr49 residues of Prx1 and engages in π-π interaction with Trp87. AZOX treatment significantly inhibited cell proliferation and activated mitochondrial apoptosis, evidenced by increased Bax/Bcl-2 ratio and Cytochrome C (Cyto C) release, which was accompanied by comprehensive mitochondrial dysfunction including structural damage, complex III suppression, elevated mtROS, reduced MMP, and inhibited energy metabolism. Critically, both Trp87 and Thr90 mutations substantially attenuated AZOX's effects on mitochondrial integrity and apoptotic induction. Conclusion: AZOX may bind to the Trp87 and Thr90 sites of Prx1 to inhibit mitochondrial function and energy metabolism, and induce mitochondria-mediated apoptosis, thereby suppressing the progression of OLK.
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