142 VITAMINS A AND CAROTENES 



sin) in the retinal rod cells. The impact of light upon the retinal rods ini- 

 tiates a reversible process involving the breakdown of rhodopsin (visual 

 purple) to a yellow compound of retinene (vitamin A aldehyde) and opsin 

 (a specific protein of the retina), and subsequent spontaneous resynthesis 

 of rhodopsin from these two substances. However, during this cycle some 

 of the retinene breaks away from its combination with opsin and decom- 

 poses to colorless vitamin A and to compounds without vitamin A activity. 

 This necessitates reformation from stores of vitamin A in the pigmented 

 epithelium of the retina, the blood, and body tissues generally. When the 

 latter are deficient, resynthesis of visual purple is delayed and is reflected 

 in impaired visual adaptation of the individual to dim light. A recent report 

 by Wald^ presents evidence that enzymatic reactions in the visual purple 

 cycle involve a retinene reductase system in which cozymase (DPN) acts 

 as a coenzyme. Since nicotinamide, the antipellagra factor, is an essential 

 component of cozymase, a second vitamin is implicated in this visual 

 process. Wald also states that alcohol dehydrogenase from liver can substi- 

 tute for the retinene reductase of retinal extracts. This suggests that fur- 

 ther clarification of these enzymatic reactions may provide the key to the 

 basic functions of vitamin A in epithelial cells in general and the underlying 

 causes of keratinizing metaplasia. 



2. Measurement of Night Blindness 



There is little doubt that impaired dark adaptation represents the earliest 

 physiologic manifestation of vitamin A deficiency. However, since febrile 

 states, generalized infections, and acute illnesses may also impair rod vision, 

 it is not pathognomonic of the deficiency state. Evaluation of dark adapta- 

 tion by various types of adaptometers and biophotometers has led to rather 

 discordant results. These appear to be due in part to differences inherent 

 in the physical instruments and in their use, and in part to variations 

 among individuals in their metabolic utilization and storage of vitamin A.' 

 When these instruments are effectively applied, it seems that a good meas- 

 ure of impaired dark adaptation is obtained, except in instances where the 

 visual defect is minimal.*' ^ The time-consuming nature of the test, com- 

 bined with the apparatus and trained personnel required, limits the useful- 

 ness of the method as a diagnostic aid. 



C. XEROPHTHALMIA AND KERATOMALACIA 



Xerophthalmia refers to a dry, roughened state (xerosis) of the conjunc- 

 tivae and cornea, often associated witii the occurrence of irregular whitish 



2G. Wald, Science 113, 287 (1951). 



^ J. J. Stern, Nutrition in Oplitluilmolosy, Nutrition Monograph Series, No. 1, 



National Vitamin Foundation, New York, (1950). 

 " P. C. Jeans, K. L. Blanchard, and F. E. Satterthwaite, J. Pcdiat. 18, 170 (1941). 

 5 R. E. Eckardt and L. V. Johnson, J. Pcdiat. 18, 195 (1941). 



