Inhibition of mitochondrial permeability transition pore is one of the mechanisms of cardioprotective effect of coenzyme Q10

: Protective properties of coenzyme Q10 (CoQ10) on the: (i) Langendorff isolated guinea pig heart's function under ischemia and reperfusion (I/R) and on the isolated mitochondria (ii) the mitochondrial permeability transition pore (MPTP) opening under exposure to calcium as natural MPTP inductor and phenylarsine oxide as oxidant--were studied. Physiological characteristic of contractile function, myocardial oxygen consumption and mitochondrial factor release as index of MPTP opening were compared before and after ischemia of isolated heart in control animals and animals with preliminary administration of CoQ10 per os. It have been shown that I/R disturbances of heart function were decreased and oxygen metabolism was normalised in animals treated with CoQ10 in compare to non-treated control. It was accompanied with substantial stabilization of mitochondrial membrane. Decreased I/R disturbances of isolated heart from CoQ10-treated animals were correlated to amount of mitochondrial factor released to coronary flow. Moreover, preliminary incubation of mitochondria, isolated from rat heart, with CoQ10 (10(-5) mol/l) substantially prevented calcium and phenylarsine-induced, cyclosporine A-sensitive mitochondrial swelling. This protective effect was increased in experiments with deenergizing mitochondria. Results of physiological and biochemical study reveal that one of the mechanisms of CoQ10's cardioprotective effect could be direct inhibition of mitochondrial permeability transition pore opening during ischemia and reperfusion of the heart.