IMMEDIATE EFFECTS OF X-RAYS ON LIVING CELLS 139 



HOLMJis: I know that the emission occm-rcd at different teini)eratiiics. hotli at 

 5° and 50°C. Prof. Mitchell's hypothesis is that one of tliese pi-ocesses is associ- 

 ated with the presence of long-hved int(>nnechary cheinical products, for instance 

 hydrogen peroxide. The other one in his opinion may be (hie to DNA molecules; 

 the energy released is passed either into the surroumhng medium or to other 

 DNA molecules. His opinion is not uiore definite than that. This is all that T 

 can t(^l] about these experiments. 



MOUTON : Is radiation damage to the cell accompanied by an increase in the lactic 

 acid content? 



HOLMES : In Dr. Forssberg's experiments a temporary rise of the lactic acid con- 

 tent was observed at a time when increase in length of the sporangiophores 

 was inhibited. Afterwards the lactic acid was removed. 



errera: I am interested in Prof. Mitchell's study. I would like to ask whether 

 you know what the emission spectrum was? 



holmes: No, I do not know that. Prof. Mitchell told me only that it was in the 

 short wave ultraviolet with unexpectedly high energies. 



powers: Which cells have you studied when nucleoli were irradiated by nucro- 

 beams of X-rays? 



HOLMES : Fibroblasts of the mouse heart. Every one of the three nucleoli in these 

 cells was irradiated. This study was made by Dr. Seed. 



barendsen: What was the irradiation applied to the nucleoli? 



HOLMES: Approximately 500 r per nucleolus. I myself have never used this 

 equipment and carmot give an exact description of it here. 



manilov : You have told us that if, after the radiation exposure, mononucleotides 

 are added, DNA synthesis continues but is delayed by 13 hr. Could you tell 

 us which nucleotides should be added and how in your opinion these nucleotides 

 penetrate into living cells and are taken up by the nucleus? 



holmes: We have never attempted experiments with nucleotides. We do not 

 know what is the cause for this delay of synthesis, but according to some in- 

 vestigators it is due to damage to the template or to some part of it in any case. 

 It is possible that the damaged part is less protected than the nucleoprotein mole- 

 cule as a whole. My personal opinion is that the delay may also be due to some 

 interference with the phosphorylation process coimected with nucleotides. Dr. 

 Looney did not administer nucleotides but only thymidine. 



Addendum to Discussion by Dr. Barbara E. Holmes 

 It is known that mitosis can be inhibited by mechanisms other than the in- 

 hibition of DNA synthesis, since a fairly small dose of X-rays will prevent cells 

 from passing into mitosis even when the dose is given after DNA synthesis has 

 been completed in those cells. We can illustrate this point with regenerating rat 

 liver, since a dose of 450 r given to the dividing tissue immediately prevented any 

 more cells from passing into mitosis— but I do not know how long this effect lasts. 

 At the other extreme 450 r given to cells before DNA synthesis had started 



