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

Irina Odinokova1, Yulia Baburina2, Alexey Kruglov3

  • 1Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Moscow 142290, Russia. odinokova@rambler.ru.

International Journal of Molecular Sciences
|June 9, 2018
PubMed

Insights

Melatonin (MEL) protects heart mitochondria from damage caused by isoprenaline hydrochloride (ISO)-induced heart failure. MEL administration reduces reactive oxygen species (ROS) production and preserves mitochondrial function, offering cardioprotection.

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Medicine
  • Pharmacology

Background:

  • Mitochondrial dysfunction, characterized by excessive reactive oxygen species (ROS) generation and permeability transition pore opening, contributes to cardiac pathologies.
  • Melatonin (MEL), a hormone with antioxidant properties, is known to enhance mitochondrial function.

Purpose of the Study:

  • To investigate the protective effects of MEL on heart mitochondria in aged rats experiencing acute cardiac failure induced by isoprenaline hydrochloride (ISO).
  • To elucidate the mechanisms underlying MEL's cardioprotective actions at the mitochondrial level.

Main Methods:

  • Histological analysis of rat heart muscle fibers.
  • Assessment of mitochondrial function, including respiratory control index (RCI) and Ca2+ retention capacity in isolated rat heart mitochondria (RHM).
  • Evaluation of protein expression of mitochondrial respiratory complex subunits and 2′,3′-cyclicnucleotide-3′-phosphodiasterase (CNPase).

Main Results:

  • MEL administration mitigated age-dependent structural damage in cardiac muscle fibers and reduced ISO-induced acute cardiac failure.
  • MEL preserved RCI and Ca2+ retention capacity while decreasing mitochondrial swelling in ISO-treated rats.
  • MEL partially prevented alterations in respiratory complexes III and V subunits and significantly reduced the expression of complex I subunit NDUFB8, inhibiting ROS production.
  • MEL maintained 2′,3′-cyclicnucleotide-3′-phosphodiasterase (CNPase) levels, which were elevated in acute heart failure.

Conclusions:

  • Melatonin effectively prevents mitochondrial dysfunction and offers cardioprotection against ISO-induced heart failure in aged rats.
  • MEL's protective effects involve the inhibition of ROS production and preservation of mitochondrial integrity.
  • Elevated levels of CNPase contribute to cardioprotection during aging and heart failure, and MEL helps maintain these levels.
Keywords:
2′,3′-cyclic nucleotide 3′-phosphodiesterase (CNPase)ROS productionacute heart failureagingmelatoninpermeability transition porerat heart mitochondriavoltage-dependent anion channel (VDAC)

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