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Research Paper|Volume 6, Issue 2|pp 140—148

Antioxidant SkQ1 delays sarcopenia-associated damage of mitochondrial ultrastructure

Valeriya B. Vays1,2, Chupalav M. Eldarov1, Irina M. Vangely1,2, Nataliya G. Kolosova2,3, Lora E. Bakeeva1,2, Vladimir P. Skulachev1,2
  • 1Lomonosov Moscow State University, Belozersky Institute of Physico-chemical Biology, Vorobyevy Gory, Moscow 119992, Russia
  • 2Lomonosov Moscow State University, Institute of Mitoengineering, Vorobyevy Gory, Moscow 119992, Russia
  • 3Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, Acad., Novosibirsk 630090, Russia
Received: December 26, 2013Accepted: February 3, 2014Published: February 5, 2014

Copyright: © 2014 Vays et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

A comparative electron-microscopic study of ultrastructure of mitochondria in skeletal muscles of the 3- and 24-month-old Wistar and OXYS rats revealed age-dependent changes in both general organization of the mitochondrial reticulum and ultrastructure of mitochondria. The most pronounced ultrastructure changes were detected in the OXYS rats suffering from permanent oxidative stress. In the OXYS rats, significant changes in mitochondrial ultrastructure were detected already at the age of 3 months. Among them, there were the appearance of megamitochondria and reduction of cristae resulting in formation of cristae-free regions inside mitochondria. In the 24-month-old OXYS rats, mitochondrial reticulum was completely destroyed. In the isotropic region of muscle fiber, only small solitary mitochondria were present. There appeared regions of lysed myofibrils as well as vast regions filled with autophagosomes. A mitochondrial antioxidant SkQ1 (given to rats with food daily in the dose of 250 nmol/kg of body weight for 5 months beginning from the age of 19 months) prevented development of age-dependent destructive changes in both the Wistar and OXYS rats.