We demonstrated that O3 treatment induced the activation of a plasma membrane anion channel that is an early prerequisite of O3-induced cell death in A. thaliana.
It was found that an O3 challenge induced the activation of a plasma membrane anion channel which was an early prerequisite of O3-induced cell death in A. thaliana.
However, our data are the first direct evidence that O3 can regulate anion channel activity and that this anion current increase is an early prerequisite to the morphological and biochemical events participating to PCD.
Indeed, several studies have reported that in various types of mammalian cells, the activation of a plasma membrane Cl− channel is an early prerequisite to apoptotic events including cell shrinkage (termed AVD for apoptotic volume decrease), cytochrome c release, the activation of proteases (including caspases) and nucleases and, ultimately, cell death [38], [39].
In various mammalian cell types, AVD, which is mediated by water loss caused by activation of anion channels and a K+ outward rectifying channel, is an early prerequisite to apoptotic events including cell shrinkage, cytochrome c release, activation of proteases (including caspases) and nucleases, and ultimately PCD [39], [64].
It is an early prerequisite for the activation of caspases.
The reduction of MMP is early prerequisite step toward apoptosis.
Cell migration is an early prerequisite for tumor metastasis with enormous impact on patient prognosis [ 23].
As the eNOS-mediated generation of NO appears to be an early event prerequisite for the induction of survivin, we studied controls (group NI) and animals after noise exposure (90 dB for 1 h, group NIII).
If it should be clear already earlier that the prerequisites for performing these experiments are fulfilled, this second sequence of tests can already be started earlier on in the mission.
