Carabrone
is isolated from Carpesium macrocephalum Franch. et Sav, which has good fungicidal activity, especially for Gaeumannomyces graminis (Get). According
to previous studies, we speculated that carabrone targets the mitochondrial
enzyme complex III of Get. To elucidate the mode
of action, we used carabrone to induce oxidative stress and apoptosis
in Get. Incubation with carabrone reduced the burst
of reactive oxygen species (ROS) and mitochondrial membrane potential,
as well as phosphatidylserine release. Carabrone caused ROS accumulation
in mycelia by inhibiting the activity of antioxidase enzymes, among
which inhibition of glutathione reductase (GR) activity was most obvious.
The catalytic center of GR consists of l-cysteine residues
that react with the α-methylene-γ-butyrolactone active
site of carabrone. Additionally, a positive TUNEL reaction led to
diffusion of the DNA electrophoresis band and upregulation of Ggmet1 and Ggmet2. We propose that carabrone
inhibits antioxidant enzymes and promotes ROS overproduction, which
causes membrane hyperpermeability, release of apoptotic factors, activation
of the mitochondria-mediated apoptosis pathway, and fungal cell apoptosis.