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Tamás König András Kapus Balázs Sarkadi 《Journal of bioenergetics and biomembranes》1993,25(5):537-545
The effect of equisetin, an antibiotic produced byFusarium equiseti, has been studied on mitochondrial functions (respiration, ATPase, ion transport). Equisetin inhibits the DNP-stimulated ATPase activity of rat liver mitochondria and mitoplasts in a concentration-dependent manner; 50% inhibition is caused by about 8 nmol equisetin/mg protein. The antibiotic is without effect either on the ATPase activity of submitochondrial particles or on the purified F1-ATPase. It inhibits both the ADP- or DNP-activated oxygen uptake by mitochondria in the presence of glutamate + malate or succinate as substrates, but only the ADP-stimulated respiration is inhibited if the electron donors are TMPD + ascorbate. It does not affect the NADH or succinate oxidation of submitochondrial particles. Equisetin inhibits in a concentration-dependent manner the active Ca2+-uptake of mitochondria energized both by ATP or succinate without affecting the Ca2+-uniporter itself. The antibiotic inhibits the ATP-uptake by mitochondria (50% inhibition at about 8 nmol equisetin/mg protein) and the Pi and dicarboxylate carrier. It does not lower the membrane potential at least up to 200 nmol/mg protein concentration. The data presented in this paper indicate that equisetin specifically inhibits the substrate anion carriers of the mitochondrial inner membrane.Abbreviations EGTA
ethyleneglycol bis/-aminoethylether/-N, N-tetraacetic acid
- DNP
2, 4-dinitrophenol
- TMPD
N,N,N,N,tetramethyl-p-phenylenediamine
- CCP
carbonylcyanide-m-chlorophenyl hydrazone
- TPP
tetraphenyl-phosphonium
- Hepes
/4,(2-hydroxyethyl)-1-piperazine-ethanesulfonic acid/ 相似文献
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