330 CONTROL OF BIOLUMINESCENGE 



gaseous diffusion into the photogenic tissue. However, the volume of 

 the tracheoles is neghgible compared with that of the tissues, and the 

 final effect of oxygen limitation would in any case be seen in the 

 cytoplasm and must involve diffusion of oxygen in solution. Hence, 

 some reason must be given why dissolved oxygen will not diffuse into 

 the photogenic tissue from the surroimding and presumably well- 

 oxygenated blood, and from contiguous tissues. Furthermore, the 

 slowness of diffusion of dissolved gases, particularly at the very low 

 p02 and small gradients at which limitation would occur during the 

 decay phase of luminescence, raises serious doubt that the observed 

 time constants for the flash could be achieved. End-cell control was 

 examined exhaustively in my 1948 review, and the conclusion was 

 reached that control at the enzymatic level, probably via nervous 

 tiiggering, was much more likely — a notable piece of clairvoyance, in 

 view of Dr. McElroy's recent ingenious acetylcholine proposal. 



The effects of different oxygen tensions on the luminescence of in- 

 tact fireflies (Snell, 1932; Alexander, 1943; Buck, 1948) bring up 

 another facet of the control problem. Normally, captive fireflies do 

 not luminesce visibly while at rest, but if the ambient p02 is gradu- 

 ally reduced to about 4 mm, an "hypoxic glow" (not a flash) develops, 

 which persists steadily for a long time. If the pOo is suddenly in- 

 creased, the luminescence suddenly increases to a high level and 

 then declines to zero ("pseudoflash"). If the p02 is decreased still 

 further, the hypoxic glow dies out. These phenomena have been 

 interpreted in terms of a control mechanism which is inactivated at 

 low pOo, allowing oxygen to diffuse into the photogenic tissue 

 unchecked but producing only a dim light because of the low pOo. 

 The pseudoflash, on this interpretation, would represent a period of 

 bright luminescence due to the increased pOo and terminated quickly 

 by the recovery of the control mechanism. (The die-out with decrease 

 in pOo below 4 mm would of course signify a straight oxygen limita- 

 tion.) 



Snell (1932) interpreted the control mechanism directly in terms 

 of the end cell, and I (1948) suggested the possibility of the pseudo- 

 flash being due to burn-off of luciferin accumulating during hypoxia 

 as in the bacterial "flash" (according to Dr. McElroy's present firefly 

 scheme this would represent oxidation of accumulated "active inter- 



