RESPIRATION OF BARLEY PROTOPLASTS BEFORE AND AFTER ILLUMINATION

Respiratory O-2 consumption was investigated in dark-adapted barley (H ordeum vulgare L. cv. Gunilla) protoplasts and after illumination for 10 min at high and very low CO2 in the presence of respiratory and pho torespiratory inhibitors. In dark-adapted protoplasts no difference wa s observed between inhibitor treatments in high and very low CO2. The respiratory rate increased somewhat after illumination and a differenc e in responce to inhibitors was in some cases observed between high an d very low CO2. Thus, the operation of the mitochondrial electron tran sport chain is affected following a period of active photosynthesis. I n all situations tested, oligomycin inhibited respiratiory O-2 uptake indicating that respiration of mitochondria in protoplasts is not stri ctly ADP limited. Antimycin A inhibited respiration more in dark-adapt ed protoplasts than after illumination whereas SHAM gave the opposite response. Rotenone inhibited respiration both in dark adapted protopla sts (about 30%) and after illumination where the inhibition was much g reater in very low CO2 (50%) than in high CO2 (10%). After iiluminatio n in very low CO2, SHAM + rotenone inhibited respiration almost comple tely (70%). Photorespiratory inhibitors had very small effect on O-2 c onsumption in darkness. After illumination the effect of aminoacetonit rile (AAN) was also very low whereas a-hydroxypyridine-2-methane sulph onate (HPMS) in photorespiratory conditions inhibited O-2 uptake much stronger (35%). The addition of glyoxylate enhanced respiration in the presence of HPMS up to the control level suggesting that alternative pathways of glyoxylate conversion might be operating. The differences in inhibitor responses may reflect fine mechanisms for the regulation of energetic balance in the plant cell which consists of switching fro m electron transport coupled to ATP production to non-coupled transpor t. Photorespiratory flux is also very flexible, and the suppression of glycine decarboxylation can induce bypass reactions of glyoxylate met abolism.