Although the MPTP has been studied mainly in mitochondria from mammalian sources, mitochondria from diverse species also undergo a similar transition. While its occurrence can be easily detected, its purpose still remains elusive.  Some have speculated that the regulated opening of the MPT pore may minimize cell injury by causing ROS-producing mitochondria to undergo selective lysosome-dependent mitophagy during nutrient starvation conditions. Under severe stress/pathologic conditions, MPTP opening would trigger injured cell death mainly through necrosis.
There is controversy about the question of whether the MPTP is able to exist in a harmless, "low-conductance" state. This low-conductance state would not induce MPT and would allow certain molecules and ions to cross the mitochondrial membranes. The low-conductance state may allow small ions like Ca to leave mitochondria quickly, in order to aid in the cycling of Ca in healthy cells. If this is the case, MPT may be a harmful side effect of abnormal activity of a usually beneficial MPTP.
MPTP has been detected in mitochondria from plants, yeasts, such as Saccharomyces cerevisiae, birds, such as guinea fowl and primitive vertebrates such as the Baltic lamprey. While the permeability transition is evident in mitochondria from these sources, its sensitivity to its classic modulators may differ when compared with mammalian mitochondria. Nevertheless, CsA-insensitive MPTP can be triggered in mammalian mitochondria given appropriate experimental conditions strongly suggesting this event may be a conserved characteristic throughout the eukaryotic domain.