Ca2+-dependent depolarization of energized mitochondrial membrane potential by chlortetracycline (aureomycin).

Abstract

The addition of chlortetracycline (CTC) to succinate-energized rat liver mitochondria resulted in depolarization of the membrane potential and decreased respiratory control. CTC inhibited both processes at concentrations that were half maximally effective at approximately 13 and 16 microM, respectively. These inhibitory effects were prevented by either the Ca2+ chelator, ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, or the inhibitor of mitochondrial Ca2+ influx, ruthenium red. These findings are consistent with the formation of a membrane associated calcium-CTC complex and suggest that CTC can alter mitochondrial energy metabolism during transmembrane Ca2+ cycling.