Abstract
The respiratory fractionation of stable oxygen isotope by Catharanthus roseus cells during Pi uptake indicated that whereas H+/Pi symport stimulated oxygen uptake only 18%, it dramatically increased the engagement of alternative pathway respiration (APR) from 12 to 79%. Despite the large engagement of APR, nPG inhibited only the Pi-stimulated portion of the oxygen uptake and turned the uninhibited portion engaged in cytochrome pathway respiration (CPR) without affecting Pi uptake. Similarly, cyanide inhibited only the Pi-stimulated portion and shifted the uninhibited remainder to APR, but severely inhibited Pi uptake. These respiratory changes were associated with a severe inhibition of protein synthesis due to the symport-induced cytoplasmic acidosis. The massive engagement of APR during the symport or the subsequent nPG-induced reengagement of CPR (uncoupled) functions as ingeniously controlled overflow of the reducing equivalents that exceed the demand by ATP-utilizing process (Pi uptake), in other words, as intracellular pH and redox homeostatic mechanism.
