Mildronate protects heart mtDNA from oxidative stress toxicity induced by exhaustive physical exercise

Arch Biochem Biophys. 2021 Jul 15:705:108892. doi: 10.1016/j.abb.2021.108892. Epub 2021 Apr 27.

Abstract

Exhaustive physical exercises are potentially dangerous for human's physical health and may lead to chronic heart disease. Therefore, individuals involved in such activity require effective and safe cardioprotectors. The goal of this research was to study Mildronate (a cardioprotective drug) effect on the level of oxidative stress markers in hearts of mice under conditions of exhausting physical exercise, such as forced swimming for 1 h per day for 7 days. Forced swimming lead to mtDNA damage accumulation, increase in diene conjugates level and loss of reduced glutathione despite an increase in antioxidant genes expression and activation of mitochondrial biogenesis. Mildronate treatment reduced oxidative stress, probably due to the inhibition of fatty acids transport to mitochondria and an increase in the intensity of glucose oxidation, which in part confirms by increase in glucose transporter expression. Thus, we can assume that Mildronate is an effective cardioprotector in exhaustive physical exercises.

Keywords: Exhaustive physical exercise; Mildronate; Mitochondria.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Cytoprotection / drug effects
  • DNA, Mitochondrial / metabolism*
  • Male
  • Methylhydrazines / pharmacology*
  • Mice
  • Mitochondria, Heart / drug effects*
  • Mitochondria, Heart / metabolism*
  • Oxidative Stress / drug effects*
  • Physical Conditioning, Animal / adverse effects*

Substances

  • Antioxidants
  • DNA, Mitochondrial
  • Methylhydrazines
  • 3-(2,2,2-trimethylhydrazine)propionate