518 RADIATION HIOLOGY 



This has boon iiichulcil in the schcinc without any commit incut as to the 

 nature of the Hj;ht al)sorher or tlie dilator substance. 



On the left of the scheme, injury to the minute vessels of the dermis is 

 indicated as resultinjj; in inhibition of their dilation. It may be supposed, 

 in :icct)rilance with the aij^unAciit ahcady jjresented, that the underlying 

 photochemical changes are essentially the same as those which result in 

 (>rythema but that they occur at a different locus. It is suggested that 

 injury to epidermal cells and to the vessels of the dermis may both be con- 

 cerned in the dilation of vessels immediately adjacent to the area exposed 

 to ultraviolet radiation, which manifests itself grossly as the delayed flare. 



The various aspects of sunburn are essentially similar to those of inflam- 

 matory responses in general. Menkin (1940, 1942, 1943a, b, 1944) has 

 succeeded in isolating from inflammatory exudates several substances 

 which he concludes act specifically in bringing about certain of the tissue 

 responses characteristic of inflammation. It seems not unlikely that the 

 complicated picture presented by inflammation may ultimately be 

 analyzed in terms of such "inflammation substances," and this general 

 thesis has been follow^ed in the scheme shown in Fig. 13-1 1 where the elab- 

 oration of a number of such substances is indicated as resulting from 

 injury to the epidermal cells. According to Menkin, the increase in capil- 

 lary permeability which occurs in inflammation is not due to histamine as 

 supposed by Lew'is and others but to a substance which he calls "leuko- 

 taxine." This substance also exerts a chemotactic effect, and, by virtue 

 of both these actions, brings about the migration of the leukocytes from 

 the capillaries into the surrounding tissues. In the present scheme leuko- 

 taxine is credited with bringing about the migration of leukocytes and 

 with tissue edema, the latter being a direct result of increased capillary 

 permeability. Indicated by a dotted line in the diagram is the probable 

 participation of vasodilation as a lesser factor in the edema. 



Cellular degeneration in the epidermis, followed by proliferation, is indi- 

 cated as resulting directly from injury to the epidermal cells by the pri- 

 mary photochemical reaction. Alternatively, there is indicated the 

 formation of other intermediary substances which may cause such cellular 

 degeneration and proliferation. The substance necrosin, w^hich Menkin 

 (1943b) finds to cause the degeneration of cells, may be responsible in part 

 for such changes in the epidermis and w^ould be included in this category. 

 It should be emphasized that none of these mediating substances has as 

 yet been isolated from sunburned skin. 



Consistent with the rest of the scheme, there has been introduced, as 

 one of the products of the injury to epidermal cells, a " melanotactic " 

 factor which contributes a part of the melanization of the epidermis that 

 becomes manifest as suntan. This melanotactic factor presumably 

 accounts for the migration of the melanin i)igment which is observed in 

 the early stage of the melanization process. The existence of such a sub- 



