Relationship between the inhibition of leaf respiration by light and enhancement of leaf dark respiration following light treatment

Respiration (R, non-photorespiratory mitochondrial CO2 release) in leaves is inhibited by light. However, exposure to darkness after a period of illumination can also result in R being temporarily stimulated (termed 'light enhanced dark respiration', LEDR). We used a fast-response CO2 exchange system to investigate these observations in tobacco leaves. After switching off the light, there were two peaks of CO2 release, the first at 15-20 s (the photorespiratory post-illumination burst) and the second at 180-250 s (LEDR). LEDR occurred in all post-illumination experiments, independent of O-2 or CQ(2) concentration. However, LEDR increased with increasing irradiance during the pre-dark period, suggesting some dependency on prior photosynthesis. We investigated the inhibition of R by light at low CO2 concentrations (Gamma(*)): Gamma(*) is the intercellular CO2 concentration at which net CO2 release represents R in the light. The inhibition of R in the light took about 50 s and was even evident at 3 mu mol photons m(-2) s(-1), regardless of the light quality (red, blue or white). The inhibition of R by light showed similar dependency on irradiance as LEDR, such that the degree of inhibition was positively correlated with the level of LEDR. In the light, switching from 350 ppm to a low CO2 concentration that resulted in the intercellular CO2 concentration being at Gamma(*), resulted in R initially increasing and then stabilising. Maintaining the leaf at Gamma(*) did not, therefore, lead to an underestimation of R. Our data suggest that a common mechanism may be responsible for both the inhibition of R by light and LEDR.