Mechanisms of creatine kinase release from isolated rat skeletal muscles damaged by propylene glycol and ethanol.
The organic cosolvents propylene glycol and ethanol are found to cause skeletal muscle damage and creatine kinase release following intramuscular injection. The mechanisms of this organic cosolvent-induced enzyme release have not been elucidated. Cosolvent-induced creatine kinase release was enhanced by the addition of calcium to the incubation medium, and inhibited, albeit modestly, by dibucaine, a nonspecific phospholipase A2 inhibitor. The temporal pattern of creatine kinase release further suggested that cosolvent-induced enzyme release from skeletal muscles may be caused by an intracellular mechanism rather than by a direct solubilization of sarcolemma. This intracellular mechanism may involve the mobilization of calcium.
Brazeau
G A
GA
Department of Pharmaceutics, School of Pharmacy, State University of New York, Buffalo 14260.
Fung
H L
HL
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D003402:Creatine Kinase / Q000378:metabolism*; D003992:Dibucaine / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009132:Muscles / Q000187:drug effects / Q000201:enzymology*; D019946:Propylene Glycol; D011409:Propylene Glycols / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012508:Sarcolemma / Q000187:drug effects
D011409:Propylene Glycols; D000431:Ethanol; D019946:Propylene Glycol; D003402:Creatine Kinase; D003992:Dibucaine; D002118:Calcium