Abstract
Chloramphenicol (CAP) inhibited tobacco cell growth as shown by a reduction (34%) of cell mass 4 days after treatment. The rates of cell respiration were slightly higher than control under coupled conditions. However, CAP‐treated cells showed a decreased maximal capacity of the cytochrome pathway (48%) and an increased maximal capacity of alternative path (56%) 4 days after treatment. In purified mitochondria, the rates of NADH or malate oxidation under state 4 conditions were not significantly changed by CAP treatment. However, the state 3 rates were 34–40% lower in CAP‐treated than in control mitochondria. Succinate oxidation decreased by 31–46% under both state 4 and state 3 conditions after CAP treatment. The activities of complexes I, III, and IV, which contain mitochondrially encoded subunits, decreased by about 50% in CAP‐treated mitochondria. There was also a decrease in the contents of mitochondrial cytochromes. Unexpectedly, the activities of complex II and the matrix‐facing rotenone‐insensitive NADH dehydrogenase, which are thought to be nuclear‐encoded, also declined. The activities of external NADH dehydrogenase, NAD‐linked malic enzyme, and fumarase remained unchanged after CAP treatment. There was a slight increase in the activity and protein level of alternative oxidase. An electrochemical gradient across the mitochondrial membranes was observed by Rhodamine 123 staining in CAP‐treated cells. However, the morphology of most of the mitochondria changed from spherical to vermicular. A method for purifying a high yield of intact mitochondria from tobacco cell suspension cultures is described.
Published Version
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