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.
Highlights
Sarcopenia, the gradual loss of muscle mass and function, is a common feature of human aging
The molecular mechanisms leading to sarcopenia are not completely identified, but the retardation of an oxidative damage entailed with an age-linked mitochondrial dysfunction occurring in the muscle cells looks as promising approach to treat this disease
As was previously shown using three-dimensional reconstitution of ultrathin serial sections [26,27,28,29], the mitochondrial profiles in skeletal muscles are united to the mitochondrial reticulum stretching along the muscle fiber
Summary
Sarcopenia, the gradual loss of muscle mass and function, is a common feature of human aging. The molecular mechanisms leading to sarcopenia are not completely identified, but the retardation of an oxidative damage entailed with an age-linked mitochondrial dysfunction occurring in the muscle cells looks as promising approach to treat this disease. Mitochondrial ROS production associated with a dysfunction of respiratory chain complexes has been implicated in a number of degenerative diseases and biological aging [3,4,5,6,7,8,9,10,11,12].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
