(41
C) were previously shown to inactivate photosystem II (PS II) in Chlorella pyrenoidosa Chick, strain CALU-175. These treatments also increased chloroplast respiration by 7–11 times. At the same time, any
attempt to inhibit the accumulation of substrates for chloroplast respiration (CO2 deprivation during nitrogen
starvation, inhibition of glucose metabolism by a nonmetabolizable analog of glucose, 2-deoxy-D-glucose, or
inhibition of protein synthesis by cycloheximide during dark incubation on glucose or by heat shock) prevented
the stimulation of chloroplast respiration and PS II inactivation. Inhibition of the oxygen-dependent oxidation
of the plastoquinone pool under anaerobic conditions or in the presence of salicylhydroxamate, an inhibitor of
chloroplast oxidases, markedly increased the extent and rate of PS II inactivation in cells subjected to heat
shock. The dependencies of chloroplast respiration and the PS II inactivation rate on the heat-shock temperature
exactly matched one another. Diuron, an inhibitor of photosynthetic electron transport between the primary and
secondary quinone electron acceptors, did not affect the rate of chloroplast respiration, but prevented PS II inac-
tivation. We propose that the inactivation of PS II caused by these treatments is due to the loss of the primary
quinone electron acceptor as a consequence of its two-electron reduction from the plastoquinone reduced by
the electron flow from the substrates of chloroplast respiration.