THE PHOTORECEPTOR PROCESS IN VISION 



689 



diet, some subjects immediately begin to become 

 night-blind, whereas others show no effects, visual 

 or otherwise, for many months; and //) on admin- 

 istration of vitamin A to night-blind subjects, some 



^ 





10 10 30-0 10 iO JO 



pre-diet -DAYS -on diet 



FIG. 22. Thresholds of completely dark -adapted cones 

 and rods during 30 days of heavy vitamin .\ administration 

 (Jejt) and during 30 days on a vitamin .'\-deficient diet (jight"). 

 Open and closed circles show thresholds of right and left eyes, 

 respectively. On the thirtieth day of the deficient diet, one 

 dose of vitamin A was administered; both rod and cone thresh- 

 olds returned to normal. On the thirty-second day, the subject 

 was again slightly night-blind and was given a dose of carotene, 

 again both cone and rod thresholds returned to normal. 

 [From VVald et al. C77).] 



are cured completely within several hours, whereas 

 others retain some degree of night blindness for 

 months while recei\ing a high dosage of vitamin A. 

 Figure 22 shows the rapid type of onset of night blind- 

 ness, figure 23 the rapid type of cure. Unfortunately 

 the other type of result is observed at least as often 

 (28, 35, 66). 



One must distinguish an acute from a chronic 

 syndrome in \itamin A deficiency. The results of a 

 current study ot vitamin A deficiency in the rat are 

 summarized in figure 24 (cf. 12a). When an animal 

 is placed on a vitamin A-deficient diet, the liver stores 

 slowly lose \itamin A until the liver has been emptied. 

 Up to this time the blood level remains normal, but 

 now it sinks within a few days to zero. To this point 

 the rhodopsin content of the retina has remained nor- 

 mal, but now this too falls, marking the beginning of 

 night blindness. For about three weeks longer the opsin 

 level stays normal. Then it too begins to fall; at the 

 same time the retina deteriorates anatomically, and 

 the animal loses weight and displays other overt signs 

 of vitamin A deficiency. All these disorders are reversed 

 by administration of \itamin A. 



The role of vitamin A as the precursor of visual 

 pigments seems almost trivial coinpared with its 

 general role in maintaining the integritv of the 

 tissues. The mechanism of this action is still com- 

 pletely obscure. In vitamin A deficiencv, various 

 tissues all over the bod\ begin to deteriorate, the 



ao )oo 



mi n i/fes 



FIG. 23. The cure of night-blindness with carotene. Following a standard light adaptation, the 

 measurement of dark adaptation shows both cone and rod plateaus to lie abose their normal range 

 (enclosed within the upper and lower pairs of broken lines^. After dark adaptation was completed, 20,000 

 International Units of carotene in oil were administered in gelatin capsules orally. For 12 to 14 

 min. the rod threshold remained constant; then it fell rapidly to normal. Immediate repetition of 

 the standard adaptation procedure showed both cone and rod plateaus to have entered their normal 

 ranges. [F'rom Wald & .Steven (78).] 



