ANNUAL REPORT, 1939 71 



DEPARTMENT OF HOME ECONOMICS NUTRITION 



Helen S. Mitchell in Charge 



Cause and Control of Nutritional Cataract. (H. S. Mitchell, G. M. Cook, 

 O. A. Merriam, and A. W. W'ertz; Graduate Assistants: Gertrude J. Hadro, 

 Mary D. Henderson.) The study of the biochemistry of cataract continues to 

 be the major project in this department. While the experimental cataract pro- 

 duced by feeding galactose to rats may not be exactly like certain types of human 

 cataract, it is sufficiently similar to justify further stud\" of factors which may 

 hasten or delay its development. In the course of this study unexpected met- 

 abolic interrelationships have appeared and where possible these also have been 

 studied in an effort to better understand the influence of other dietary factors 

 upon carbohydrate metabolism. The results of all this animal research may 

 ultimately suggest some clinical applications. This method of producing experi- 

 mental cataract in rats in a few weeks was discovered in 1935 and has since then 

 served as a unique approach to the study of a little-understood pathologic phen- 

 omenon. 



1. The Effect of Nitrogenous Factors on the Cataractogenic Action of Galactose. 

 Since it has been established by earlier work in this laboratory that a protein 

 deficiency aggravates cataract development, and that a liberal supply delays it, 

 the question naturally arises as to what factor in protein is responsible for this 

 protective action. The relatively minor differences noted between proteins from 

 widely varied sources, mentioned in the last Annual Report, gave almost no clue 

 to the nature of the factor responsible for the inhibition of lenticular change. 

 The observations with cystine previously reported were followed by a limited 

 number of experiments with methionine. Neither of these sulfur-containing 

 amino acids fed as supplements to a 15 percent protein ration afi"orded protection 

 against cataract commensurate with protection given by adding protein yielding 

 an equivalent amount of these amino acids. The negative results obtained with 

 massive doses of thiamin chloride, riboflavin, yeast, and ascorbic acid, as well 

 as the excellent condition of the animals, offer convincing evidence that no known 

 vitamin deficiency is concerned. Nitrogenous products such as urea and choline 

 have been fed as supplements to the galactose ration with essentially negative 

 results. Work now in progress is concerned with the feeding of proteins treated 

 in various ways which are known to alter the nutritive value of protein for growth. 

 Thus the problem is still unsolved as to why and how protein or some fraction 

 thereof can function to inhibit lenticular changes in rats in the presence of a high 

 blood galactose. 



2. The Effect of Calcium Salts on the Utilization of Lactose. Considerable 

 variation has been observed in this laboratory in the effect of different calcium 

 salts on the digestion and absorption of lactose. Rats were fed an adequate 

 ration containing 60 percent lactose, plus 1.0 or 0.5 percent of calcium added in 

 the foim of six different calcium salts: respectively, tricalcium phosphate, carbon- 

 ate, citrate, lactate, levulinate, and gluconate. Rats on any of the first five calcium 

 salts showed as good growth as those on the plain 60 percent lactose ration, less 

 diarrhea in general, about the same degree of galactemia, and a similar incidence 

 of cataract. With calcium gluconate fed at the 1.0 percent calcium level, few 

 rats survived; these grew but little, had severe diarrhea, low blood sugar, and no 

 lenticular changes. With 0.5 percent calcium as the gluconate, survival was 

 better, growth pooi , diarrhea moderate, lenticular changes few if any. These 

 criteria all indicate that calcium gluconate prevents most of the lactose from 

 leaving the intestinal tract. Since calciun. gluconate shows no inhibitory effect 

 upon the absorption of the tingle sugars, glucose or galactose, the problem must 



