Differential effects on energy transduction processes by fluorescamine derivatives in rat liver mitochondria.

Intact rat liver mitochondria were treated with compounds derived from the reaction of fluorescamine with various types of primary amines, including the mycosamine-containing antibiotics amphotericin B and nystatin. The effect of varying amounts of these compounds on ATPase-linked inorganic phosphate (Pi) formation on oxygen consumption, and on MgATP-linked and succinate-linked proton movements was examined. The antibiotic-fluorescamine compounds did not affect the Pi formation rate but strongly inhibited both the ATPase-linked and the succinate-linked H+ extrusion rates to approximately the same extent. The antibiotic derivatives decreased the oxygen consumption rate, but this effect was much smaller than the decrease in the respiration-dependent proton extrusion rate. The benzylamine-fluorescamine compound significantly increased the Pi formation rate, in contrast to the antibiotic analogues. The benzylamine derivative, like the antibiotic derivatives, inhibited both types of proton extrusion rates. The slight decrease in the oxygen consumption rate caused by the benzylamine derivative was significantly smaller than the corresponding decrease observed with the antibiotic derivatives. These studies, in which fluorescamine derivatives bind reversibly to mitochondria, are compared with previous studies in which fluorescamine itself binds irreversibly to mitochondria and results in a Pi formation rate increase and MgATP- and succinate-linked proton extrusion rate inhibition but has no effect on the oxygen consumption rate.