EFFECTS OF EQUISETIN ON RAT-LIVER MITOCHONDRIA - EVIDENCE FOR INHIBITION OF SUBSTRATE ANION CARRIERS OF THE INNER MEMBRANE

The effect of equisetin, an antibiotic produced by Fusarium equiseti, has been studied on mitochondrial functions (respiration, ATPase, ion transport). Equisetin inhibits the DNP-stimulated ATPase activity of r at liver mitochondria and mitoplasts in a concentration-dependent mann er; 50% inhibition is caused by about 8 nmol equisetin/mg protein. The antibiotic is without effect either on the ATPase activity of submito chondrial particles or on the purified F-1-ATPase. It inhibits both th e ADP- or DNP-activated oxygen uptake by mitochondria in the presence of glutamate + malate or succinate as substrates, but only the ADP-sti mulated respiration is inhibited if the electron donors are TMPD + asc orbate. It does not affect the NADH or succinate oxidation of submitoc hondrial particles. Equisetin inhibits in a concentration-dependent ma nner the active Ca2+-uptake of mitochondria energized both by ATP or s uccinate without affecting the Ca2+-uniporter itself. The antibiotic i nhibits the ATP-uptake by mitochondria (50% inhibition at about 8 nmol equisetin/mg protein) and the P-i and dicarboxylate carrier. It does not lower the membrane potential at least up to 200 nmol/mg protein co ncentration. The data presented in this paper indicate that equisetin specifically inhibits the substrate anion carriers of the mitochondria l inner membrane.