FATS AS ESSENTIAL DIETARY COMPONENTS 883 



cording to Richardson et al.,"^"^ the methyl esters of arachidonic and lino- 

 leic acids -were useful in counteracting the dermatitis caused l)y pyridox- 

 ine deficiency, but did not afford permanent protection. These workers 

 suggest that the unsaturated acids do not replace pyridoxine but simply 

 delay the onset of the skin symptoms. They found that pyridoxine and 

 pantothenic acid are both required. 



GroM-th inhibition in rats brought about by feeding diets containing 

 suboptimal amounts of pjTidoxal or pyridoxine is accentuated, according 

 to Sarma and associates, ^"^ when oleic acid is added to the ration. How- 

 ever, this inhibitory effect of oleate can be counteracted by giving addi- 

 tional quantities of vitamin Be. 



There has been considerable speculation as to whether or not the de- 

 ficiencies in essential fatty acid and pyridoxine are entirely similar insofar 

 as the skin symptoms are concerned. Although INIedes et al."-^^ emphasized 

 the interrelation between the two types of deficiency, these results might 

 well be interpreted to mean that two different factors are involved. Thus, 

 when the diet was lacking in both of these components, a relief from the 

 deficiency was obtained by the administration of either ethyl hnoleate or 

 of pyridoxine. However, the resulting gro^^•th response was less with 

 maximum amomits of ethj'l linoleate than when optimum doses of pyri- 

 doxine were 'given. The best results were obtained when both of these 

 components were included in the diets simultaneously. According to 

 more recent work of Beaton et al.-'^'' the inclusion of corn oil in a fat-free, 

 pyridoxine-free diet had no effect upon the rate of appearance of acrodynia, 

 but it did prevent the development of severe external deficiency symptoms. 

 Acrodjmia appeared more frequently and was more severe in male rats 

 than in the females. 



In a comprehensive study of the nature of the pj-ridoxine deficiency in 

 acrodynia, and the deficiency resulting from a diet lacking the essential 

 fatty acids, Sinclair^"* observed that the lesions in the skin of rats differ 

 in these two abnormal conditions. In EFA deficiency, the concentration 

 of pyridoxine in the bod}^ was found to be normal. Sinclair-*'^ postulates 

 that, in EFA deficiency, the failure in growth occurs because phosphatides 

 (and therefore cell membranes) cannot be formed. In pyridoxine de- 

 ficiency, however, the retardation in growth is due to interference ^^'ith 



"^"^ L. R. Richardson, A. G. Hogan, and K. F. Itschner, Univ. Missouri Agr. Expt. 

 Sta., Research Bull. S33, 3-12 (1941 ); Chem. Abst., 36, 2591 (1942). 



^ P. S. Sarma, E. E. Snell, and C. A. Elvehjem, /. Nutrition, 33, 121-128 (1947). 

 »« G. Medes, D. C. Keller, and A. Kurkjian. Arch. Biochem., 15, 19-29 (1947). 

 a>^ J. R. Beaton, J. L. Beare, and E. W. McHenry, J. Nutrition, 4S, 325-334 (1952). 

 »» H. M. Sinclair, Biochem. J., 51, xvi (1952). 



