Mellvig, S. and Tillberg, J-E. 1986. Transient peaks in the delayed luminescence from Scenedesmus obtusiusctilus induced by phosphorus starvation and carbon dioxide Cells of the unicellular green alga Scenedesmus obtusiusculus (Chod.) were starved of phosphorus for 24, 48, 72 and 96 h, and the decay kinetics of the delayed luminescence from the differently starved cells was monitored for several minutes. Cells starved for 24 h showed similar delayed luminescence decay kinetics and accumulated output of photons as control cells after excitation with white light. Two transient peaks (with several components) in the decay kinetics of delayed luminescence were observed after 48 h of phosphorus starvation but not after 72 or 96 h. The amplitude of the transient peaks varied depending on the length of the excitation period with white light and on the length of the dark period preceding light excitation. High CO, availability induced no transient peak, whereas low CO, availability induced a high transient peak. Transient peaks could not be induced by excitation with light of 660 or 680 nm and only a single transient peak developed using 700 nm light. The kinetics of the delayed luminescence was changed, and the accumulated output of photons was decreased when the pH of the medium was changed from 7.2 to 9.5, both in ceils starved for phosphorus for 96 h and in controls. The data indicate that a complicated metabolic pattem is involved in the mechanisms giving rise to the observed transient peaks in the delayed luminescence. The main factors may be a reduction in the translocation of trioses from chloroplasts, a concomitant reduction in Calvin cycle activities and changes in the amount of ATP and reducing agents available Additional key words of S-states.Calvin cycle activity, charge separation, pH, recombinations S. Meiivig (reprint requests) and

Abstract— Luminescence from synchronously cultured Scenedesmus obtusiusculus cells was measured with a high sensitivity photon counter. Recording of light emission was initiated 0.2 s after switching off actinic light. Luminescence decay was separated into two phases: one for decay to 104 pulses s‐1, the other for decay from 104 to 103 pulses s‐1. Most photons are emitted during the rapid decay to 104 pulses s‐l. Only small diurnal variations of the two phases could be observed in controls. Treatment with 3‐(3,4‐dichlorophenyl)‐1,1‐dimethylurea (DCMU) decreased both the total number of photons emitted and the time required to reach the 104 pulses s‐1 level. No diurnal rhythmicity was induced by DCMU in the first phase but DCMU induced a pronounced diurnal variation in decay time in the second phase of luminescence parallelled by a periodicity in the number of photons emitted. The results indicate that DCMU interferes with the participation of PS I in luminescence. The chlorophyll alb ratio was constant during the life cycle of the cells. No relation could be observed between luminescence and the diurnal rhythmicity in photosynthesis that is characteristic for synchronized unicellular algae.

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Delayed luminescence was measured from samples of a synchronously growing cell culture of the unicellular green alga, Scenedesmus obtusiusculus Chod., every second hour during the 24 h cell cycle under a 15/9 h lighi/dark regime. Both high (air + 2.5% CO2) and low (0.03% CO2) CO2 conditions were used. Under high CO2 conditions, while light excitation induces formation of a late (maximum reached after 10–60 s) transient peak in delayed luminescence in cells sampled after 10–16 h in the cell cycle. During most of the cell cycle low CO2 conditions stimulate a late transient peak formation. Excitation with 700 nm light, but not with 680 nm light, induces a late transient peak in delayed luminescence under high CO2 conditions. The transient peak is more or less pronounced depending on the cell stage. The variations might be due to a changing capacity for light‐induced state I/stale II transitions during the cell cycle. It is assumed that the formation of a late transient peak in delayed luminescence is due to ATP hydrolyzation and is thus favoured by a high ATP/NADPH ratio. Hydrolyzation of ATP affects the transthylakoidal ΔpH, which regulates the reverse electron flow to the plastoquinone‐pool and QA/QB, thus affecting the decay kinetics of the delayed luminescence.

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