710 RADIATION BIOLOGY 



attempted. Kuske (1940) found that extracts of various plants, includ- 

 ing parsnip and fig, produced sensitivity to light of wave lengths between 

 3340 and 3060 A, with some effect at wave lengths extending up to 

 4120 A, and concluded that the photodynamic agent was fucocoumarin 

 and related substances. Foerster and Schwartz (1939) produced sensi- 

 tivity to light in the range 3900 5000 A by application of pitch and coal 

 tar and considered that acridine and anthracene are not the only photo- 

 sensitizing agents in pitch dermatitis. 



Photosensitivity in orchard workers spraying suspensions of pheno- 

 thiazine has been reported (De Eds et al., 1940). Experiments carried 

 out by De Eds et al. suggest, however, that this sensitivity was due not 

 to contact of the phenothiazine with the skin but to oral absorption of 

 the spray, leading to production of thionol, which then reached the skin 

 via the blood stream. 



Photosensitivity after Treatment with Sulfanilarnide. It is well recog- 

 nized that some persons develop sensitivity to sunlight after treatment 

 with sulfanilamide and allied substances. The report by Rimington and 

 Hemmings (1938) that an increased formation of coproporphyrin also 

 accompanied the use of these drugs encouraged the belief that this light 

 sensitivity was due to photodynamic action by porphyrins. Blum 

 (1941b) found that the radiation to which human skin was sensitized 

 after injection of sulfanilamide was restricted to wave lengths below 

 3200 A and that molecular oxygen was not needed to evoke this response. 

 Furthermore this response was not immediate, thus resembling sunburn 

 rather than photodynamic action. Blum concluded that photosensitivity 

 due to sulfanilamide is not an example of photodynamic action but prob- 

 ably represents an increased sensitivity of the sunburn mechanism of 

 normal skin. 



Association of Photosensitivity with the Porphyrias and Hydroas. The 

 occurrence of hydroa or hydroa-like lesions in cases of congenital por- 

 phyria is still freely interpreted as porphyrin photosensitization in view 

 of the established photodynamic activity of these compounds; yet as 

 early as 1923 Garrod clearly indicated that the association of hydroa 

 and porphyria could not be explained simply in this Avay. The effects of 

 exposure to light after injection of porphyrins are of a different nature 

 from those occurring in the hydroas; even in hydroa patients it has been 

 difficult to produce the typical eruption by irradiation. The wave lengths 

 that have produced effects in successful experiments do not agree with 

 the absorption spectra of porphyrins; hydroa lesions may occur without 

 elevated porphyrin excretion; some forms of porphyria, such as acute 

 idiopathic porphyria, are not accompanied by hydroa; and in some cases 

 of hydroa bullous lesions are produced by slight trauma without exposure 

 to light. Garrod concluded, however, that sensitivity to light resulting 

 from the presence of porphyrins in the tissues must be the cause of the 



