90 D. SHUGAR 



successfully applied to the freeing of plasma products from the viruses 

 causing hepatitis and jaundice. 207e The literature on this subject has been 

 briefly reviewed recently. 39 



X. Photoreactivation 



The reversal of ultraviolet damage to a biological system by exposure to 

 visible or near ultraviolet radiation has been observed for a wide variety 

 of ultraviolet radiation effects in every type of living organism, with only 

 a few exceptions. 181 These exceptions are of considerable interest from the 

 standpoint of a general theory to account for photoreactivation (PR) and 

 have, for instance, included TMV and many bacteria. The reason for 

 previous failures to photoreactivate TMV has now been shown to be due 

 to the nature of the linkage between the RNA and protein components of 

 the virus, and infectious RNA from TMV is photoreactivable. 170 A similar 

 explanation may apply to some bacteria where the intracellular state of 

 binding of DNA may likewise inhibit PR. 



Another interpretation is suggested by the several observations cited 

 above (Section VI) with regard to the greater radiation sensitivity of some 

 DNA'S in vivo; and particularly the finding that pneumococcal transform- 

 ing DNA is much more sensitive to irradiation prior to its extraction from 

 these microorganisms, 174 which could well account for lack of PR in pneu- 

 mococci. Still another possibility is photosensitized inactivation in the 

 primary irradiation process; as in the case of X-rays, it is unlikely that PR 

 would then be possible, as illustrated by Galston's 208 failure to demonstrate 

 PR for photooxidized T6r bacteriophage. 



These examples suffice to underline the importance of investigations on 

 the reasons for the absence of PR in specific cases, 181 not only from the point 

 of view of photochemical mechanisms in vivo but also for the information 

 they may provide as to the state of the intracellular components involved. 



The earlier review of Dulbecco 209 devoted exclusively to this subject has 

 been brought up to date in an excellent and comprehensive survey by 

 Jagger. 181 Before going on to a discussion of a possible mechanism for PR, 

 it is perhaps worthwhile to summarize a few of its salient features: 



K. Habel and B. T. Sockrider, J. Immunol. 56, 273 (1947); (c) L. H. Collier, D. 

 McLean, and H. Vallet, J. Hyg. 53, 513 (1955) ; (d) H. J. Shaughnessy, A. M. Wolf, 

 M. Janota, J. L. Neal, F. Oppenheimer, A. Milzer, H. Naftulin, and R. A. Morrissey, 

 Proc. Soc. Exptl. Biol. Med. 95, 251 (1957); (e) K. B. McCall, F. H. Gordon, F. C. 

 Bloom, L. A. Hyndman, H. L. Taylor, and H. D. Anderson, ./. Am. Pharm. Assoc. 

 Sci. Ed. 46, 295 (1957). 



208 A. W. Galston, Science 111, 619 (1950). 



209 R. Dulbecco, in "Radiation Biology," (A. Hollaender, ed.), Vol. II, Chapter 12. 

 McGraw-Hill, New York, 1955. 



