The aggregation of monomers is directly correlated to mitochondrial membrane potential, and their breakdown in dying cells results in a increase of green fluorescence.
Second, increased ATP consumption causes a breakdown in mitochondrial membrane potential leading to calcium accumulation [16], which further aggravates mitochondrial dysfunction.
In either scenario, a breakdown of mitochondrial membrane potential is the consequence, followed by the release of pro-apoptotic factors and loss of mitochondrial functionality.
Thus, a breakdown of the membrane potential is most likely and could be explained by the pore forming ability of daptomycin.
Dependent on plasma treatment time reduction of recovered cells was observed with no increase of apoptotic cells, but breakdown of mitochondrial membrane potential.
A pro-necrotic effect – similar to the one of Ca2+ – can be strong opening of mitochondrial pores leading to breakdown of the membrane potential, ATP depletion, sustained Ca2+ increase and premature activation of digestive enzymes.
Instead, a large fraction of the cells undergoes necrosis via a positive Ca2+ feedback probably caused by enhanced mitochondrial pore opening, breakdown of the membrane potential and of ATP production, which hinders clearance of Ca2+.
While FACS analysis after staining with propidium iodide only visualizes the cell cycle, analysis after staining with JC-1 reveals the breakdown of mitochondrial membrane potential, which is known to be a key process during mitochondrial-dependent apoptosis.
Conversely, by studying the effect of BA on mitochondrial function, we found that incubation with BA results in an enhanced breakdown of mitochondrial membrane potential in RMS-13 cells, reaching a maximum between 8 and 12 h after BA treatment.
Some indole substances are capable of supporting electron flux through the respiratory chain, preventing the breakdown of the mitochondrial membrane potential, and decreasing electron leakage, and they thereby reduce the formation of free-radicals [12].
