1. Ergosterol depletion under bifonazole treatment induces cell membrane damage and triggers a ROS-mediated mitochondrial apoptosis in Penicillium expansum
- Author
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Deng Yan, Shixin Zhang, Litao Peng, Dongmei Li, Meng Li, Shuzhen Yang, Gang Fan, and Siyi Pan
- Subjects
Programmed cell death ,Intracellular pH ,Bifonazole ,Apoptosis ,Biology ,Mitochondrion ,Cell membrane ,chemistry.chemical_compound ,Ergosterol ,Genetics ,medicine ,Ecology, Evolution, Behavior and Systematics ,Cell Membrane ,Imidazoles ,Penicillium ,food and beverages ,Hydrogen Peroxide ,biology.organism_classification ,Mitochondria ,Cell biology ,Infectious Diseases ,medicine.anatomical_structure ,Ion homeostasis ,chemistry ,Fruit ,Penicillium expansum ,Reactive Oxygen Species ,medicine.drug - Abstract
Penicillium expansum is the causal agent of blue mold in harvested fruits and vegetables during storage and distribution, causing serious economic loss. In this study we seek the action modes of bifonazole against this pathogen. Bifonazole exhibited strong antifungal activity against P. expansum by inhibiting ergosterol synthesis. The ergosterol depletion caused damage to the cell structure and especially cell membrane integrity as observed by SEM and TEM. With increased unsaturated fatty acids contents, the cell membrane viscosity decreases and can no longer effectively maintain the cytoplasm, which ultimately decreases extracellular conductivity, changes intracellular pH and ion homeostasis. Exposure of hyphal cells to bifonazole shows that mitochondrial respiration is inhibited and reactive oxygen species (ROS) levels–including H2O2 and malondialdehyde (MDA) – are significantly increased. The functional impairment of mitochondria and cell membrane eventually cause cell death through intrinsic apoptosis and necroptosis.
- Published
- 2022