Impairment of Energy-Dependent Processes in the Muscle Tissue as a Pathogenetic Mechanism of Statin-Induced Myopathy

Administration of simvastatin was followed by a decrease in activities of superoxide dismutase and cytochrome oxidase in rat mitochondria, which attested to dysfunction of the respiratory chain. The decrease in total ATPase and Ca²⁺-ATPase activities in muscle tissue homogenates reflected impaired transport of active cations essential for muscle contraction. We conclude that abnormal relationships in the system of energy synthetic and energy-dependent processes in myocytes serve as the molecular basis for the formation of statin-induced degenerative changes.