Degeneration and subsequent regeneration of mouse skeletal muscle after a single injection of chlorpromazine: changes in mitochondrial calmitine and calcium content.

We studied experimental models capable of showing muscle degeneration and subsequent regeneration and observed the changes in calmitine, calcium uptake and calcium concentration in mitochondria during these processes. The results presented here are based on the study of mitochondria of mouse skeletal muscle after a single intramuscular injection of chlorpromazine. This drug induces myotoxic effects followed by muscle regeneration. Our results show that the muscle degeneration process, as shown by histological studies, was associated with some changes in mitochondria: a decrease in calmitine, a calcium overload and a decrease in calcium uptake; the subsequent regeneration process was associated with an increase in calmitine, a decrease in calcium concentration and an increase in calcium uptake, these 3 parameters returning to normal values. It seems that there is a correlation between a decrease in calmitine and muscle degeneration, and an increase in calmitine and muscle regeneration, as shown by our biochemical and histological observations.