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Article

Effect of Melatonin on Rat Heart Mitochondria in Acute Heart Failure in Aged Rats

1
Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Moscow 142290, Russia
2
Pushchino State Natural Science Institute, Pushchino, Moscow 142290, Russia
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(6), 1555; https://doi.org/10.3390/ijms19061555
Received: 26 April 2018 / Revised: 16 May 2018 / Accepted: 16 May 2018 / Published: 23 May 2018
Excessive generation of reactive oxygen species (ROS) in mitochondria and the opening of the nonselective mitochondrial permeability transition pore are important factors that promote cardiac pathologies and dysfunction. The hormone melatonin (MEL) is known to improve the functional state of mitochondria via an antioxidant effect. Here, the effect of MEL administration on heart mitochondria from aged rats with acute cardiac failure caused by isoprenaline hydrochloride (ISO) was studied. A histological analysis revealed that chronic intake of MEL diminished the age-dependent changes in the structure of muscle fibers of the left ventricle, muscle fiber swelling, and injury zones characteristic of acute cardiac failure caused by ISO. In acute heart failure, the respiratory control index (RCI) and the Ca2+ retention capacity in isolated rat heart mitochondria (RHM) were reduced by 30% and 40%, respectively, and mitochondrial swelling increased by 34%. MEL administration abolished the effect of ISO. MEL partially prevented ISO-induced changes at the subunit level of respiratory complexes III and V and drastically decreased the expression of complex I subunit NDUFB8 both in control RHM and in RHM treated with ISO, which led to the inhibition of ROS production. MEL prevents the mitochondrial dysfunction associated with heart failure caused by ISO. It was shown that the level of 2′,3′-cyclicnucleotide-3′-phosphodiasterase (CNPase), which is capable of protecting cells in aging, increased in acute heart failure. MEL also retained the CNPase content in RHM both in control experiments and after ISO-induced heart damage. We concluded that an increase in the CNPase level promotes cardioprotection. View Full-Text
Keywords: melatonin; permeability transition pore; rat heart mitochondria; acute heart failure; aging; ROS production; 2′,3′-cyclic nucleotide 3′-phosphodiesterase (CNPase); voltage-dependent anion channel (VDAC) melatonin; permeability transition pore; rat heart mitochondria; acute heart failure; aging; ROS production; 2′,3′-cyclic nucleotide 3′-phosphodiesterase (CNPase); voltage-dependent anion channel (VDAC)
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MDPI and ACS Style

Odinokova, I.; Baburina, Y.; Kruglov, A.; Fadeeva, I.; Zvyagina, A.; Sotnikova, L.; Akatov, V.; Krestinina, O. Effect of Melatonin on Rat Heart Mitochondria in Acute Heart Failure in Aged Rats. Int. J. Mol. Sci. 2018, 19, 1555. https://doi.org/10.3390/ijms19061555

AMA Style

Odinokova I, Baburina Y, Kruglov A, Fadeeva I, Zvyagina A, Sotnikova L, Akatov V, Krestinina O. Effect of Melatonin on Rat Heart Mitochondria in Acute Heart Failure in Aged Rats. International Journal of Molecular Sciences. 2018; 19(6):1555. https://doi.org/10.3390/ijms19061555

Chicago/Turabian Style

Odinokova, Irina, Yulia Baburina, Alexey Kruglov, Irina Fadeeva, Alena Zvyagina, Linda Sotnikova, Vladimir Akatov, and Olga Krestinina. 2018. "Effect of Melatonin on Rat Heart Mitochondria in Acute Heart Failure in Aged Rats" International Journal of Molecular Sciences 19, no. 6: 1555. https://doi.org/10.3390/ijms19061555

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