Inhibition of mitochondrial permeability transition pore is one of the mechanisms ofcardioprotective effect of coenzyme Q10
V.F.Sagach, G.L.Vavilova, O.V.Rudyk, F.V.Dobrovolsky, T.V.Shimanskaya, O.S.Medvedev
O.O.Bogomoletz Institute of Physiology, NAS of Ukraine, Kyiv.
Abstract
Protective properties of coenzyme Q10 (CоQ10) 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 CоQ10 per os . It have been shown that I/R
disturbances of heart function were decreased and oxygen
metabolism was normalised in animals treated with CоQ10 in
compare to non-treated control. It was accompanied with sub-
stantial stabilization of mitochondrial membrane. Decreased
I/R disturbances of isolated heart from CоQ10 -treated animals
were correlated to amount of mitochondrial factor released to
coronary flow. Moreover, preliminary incubation of mitochon-
dria, isolated from rat heart, with CоQ10 (10-5 mol/l) substan-
tially prevented calcium and phenylarsine–induced,
cyclosporine A-sensitive mitochondrial swelling. This protec-
tive effect was increased in experiments with deenergizing
mitochondria. Results of physiological and biochemical study
reveal that one of the mechanisms of CоQ10‘s cardioprotective
effect could be direct inhibition of mitochondrial permeability tran-
sition pore opening during ischemia and reperfusion of the heart.
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