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COMPARATIVE STUDY OF LETHAL PHOTOSENSITIZATION OF SARCINA LUTEA BY 8-METHOXYPSORALEN AND BY TOLUIDINE BLUE

^a Department of Bacteriology, University of California, Berkeley, California

ABSTRACT

MATHEWS, MICHELINE M. (Department of Bacteriology, University of California, Berkeley). Comparative study of lethal photosensitization of Sarcina lutea by 8-methoxypsoralen and by toluidine blue. J. Bacteriol. 85:322–328. 1963.—A comparative study has been made of the photo-killing of Sarcina lutea by 8-methoxypsoralen (8-MOP) and by toluidine blue. It has been found that photosensitization by 8-MOP differs from photosensitization by toluidine blue, in that it has a temperature coefficient of less than one, and that the presence of oxygen is not necessary for, and even is deleterious to, the photosensitization, the psoralen being destroyed by its presence. It has previously been shown that the presence of carotenoid pigments protects the cells of S. lutea from lethal photosensitization by toluidine blue; it was found that the presence of these pigments has no protective effect in photosensitization with 8-MOP. Studies on the lethal photosensitization of S. lutea with toluidine blue suggested that the primary sensitive site of the photokilling was the protein of the cell membrane, as manifested by the destruction of membrane enzyme activity and the regulation of permeability. It has been found that photokilling by 8-MOP has no effect on these functions. A study was made on the effect of photokilling by 8-MOP on the production of penicillin-resistant mutants as an indication of an alteration in the cellular deoxyribonucleic acid (DNA) by the psoralen. Psoralen photosensitization resulted in the development of many penicillin-resistant mutants. On the basis of the findings reported in this paper, it is suggested that photosensitization of S. lutea by 8-MOP does not reflect damage to cellular protein, as does toluidine blue, but rather damage to cellular DNA.

¹ National Science Foundation postdoctoral fellow, 1961–1962. Present address: Channing Laboratory, Mallory Institute of Pathology, Boston City Hospital, and Department of Bacteriology, Harvard Medical School, Boston, Mass.

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