12CO2 emission from different metabolic pathways measured in illuminated and darkened C3 and C4 leaves at low, atmospheric and elevated CO2 concentration
Abstract
Abstract The detection of 12 CO 2 emission from leaves in air containing 13 CO 2 allows simple and fast determination of the CO 2 emitted by different sources, which are separated on the basis of their labelling velocity. This technique was exploited to investigate the controversial effect of CO 2 concentration on mitochondrial respiration. The 12 CO 2 emission was measured in illuminated and darkened leaves of one C 4 plant and three C 3 plants maintained at low (30–50 ppm), atmospheric (350–400 ppm) and elevated (700–800 ppm) CO 2 concentration. In C 3 leaves, the 12 CO 2 emission in the light ( R d ) was low at ambient CO 2 and was further quenched in elevated CO 2 , when it was often only 20–30% of the 12 CO 2 emission in the dark, interpreted as the mitochondrial respiration in the dark ( R n ). R n was also reduced in elevated CO 2 . At low CO 2 , R d was often 70–80% of R n , and a burst of 12 CO 2 was observed on darkening leaves of Mentha sativa and Phragmites australis after exposure for 4 min to 13 CO 2 in the light. The burst was partially removed at low oxygen and was never observed in C 4 leaves, suggesting that it may be caused by incomplete labelling of the photorespiratory pool at low CO 2 . This pool may be low in sclerophyllous leaves, as in Quercus ilex where no burst was observed. R d was inversely associated with photosynthesis, suggesting that the R d / R n ratio reflects the refixation of respiratory CO 2 by photosynthesizing leaves rather than the inhibition of mitochondrial respiration in the light, and that CO 2 produced by mitochondrial respiration in the light is mostly emitted at low CO 2 , and mostly refixed at elevated CO 2 . . In the leaves of the C 4 species Zea mays , the 12 CO 2 emission in the light also remained low at low CO 2 , suggesting efficient CO 2 refixation associated with sustained photosynthesis in non‐photorespiratory conditions. However, R n was inhibited in CO 2 ‐free air, and the velocity of 12 CO 2 emission after darkening was inversely associated with the CO 2 concentration. The emission may be modulated by the presence of post‐illumination CO 2 uptake deriving from temporary imbalance between C 3 and C 4 metabolism. These experiments suggest that this uptake lasts longer at low CO 2 and that the imbalance is persistent once it has been generated by exposure to low CO 2 .