TOCOPHEROLS IX VARTOT'S METABOLIC PROCESSES 717 



chynial tissues of the ombiyo proper develops. The vascular relationship 

 between the fetal and maternal components of the placenta becomes im- 

 paired, resulting in asphyxia, starvation, and death of the fetuses. Rapid 

 necrosis and resorption of the fetuses occurs almost inmiediately, folloA\ed 

 by a gradual regression of the placenta until only a blood clot remains at 

 term. 



When \'itamin E is administered to the pregnant rat at any time during 

 the first trimester (se^-en days), fetal resorption can be pre^'ented, regard- 

 less of the nature of the earlier diet. When the dosage of tocopherol is 

 critical, dehverj' of dead as well as of viable fetuses occurs, and none sur- 

 vives more than a few daj'S. WTien the dosages of a-tocopherol are in- 

 adequate, fetal death and resorption occur later than the twelfth day. 

 Mason"'-*'-29 observed that, under such conditions, fetuses exhibit changes 

 in the vascular s^'stem on about the sixteenth day of gestation, which 

 involve stasis, "vasodilation, congestion, and local hemorrhages; there is a 

 general ischemia prior to death. 



When female rats are maintained on a low-vitamin E intake after the 

 early months of life, a progressive increase in the xdtamin E requirements 

 for successful pregnancies ensues. HoweA'er, the female is able to complete 

 a satisfactory pregnancy when adequate amounts of \'itamin E are aA'ail- 

 able, even if fetal resorption has occurred in the earher pregnancies as a 

 result of an inadequate intake of A-itamin E. With increasing age, there 

 is a progressive interference with implantation of the ovum.'^°~-^- Harris 

 and co-workers^^ agree vnth the opinion of Blandau et al.-^^ that the dys- 

 function in a^-itaminosis E is uterine rather than ovarian. 



Fetal death and resorption occur in a number of different species when 

 the \dtamin E intake is too restricted. The results in the mouse-^---^^ 

 and those in the hamster^i^ are quite comparable to those in rats. Suoma- 

 lainen-^^ attributed the results in female mice to an impaired production of 

 histotrophe. Pappenheimer and Goettsch,^^^ who observed resorption in 

 the case of guinea pigs, considered the condition to be due to necrosis of 



2» K. E. Mason, Yale J. Biol. Med., 14, 605-617 (1942). 



*29 K. E. Mason, A Hemorrhagic State in the Vitamin E-Deficient Fetus of the Rat, 

 Essays in Biology (in honor of H. M. Evans), Univ. of California Press (1943), pp. 401- 

 407. 



^^ G. A. Emerson and H. M. Evans, /. Nutrition, 18, 501-506 (1939). 



"1 H. Kaunitz and C. A. Slanetz, Proc. Soc. Exptl. Biol. Med., 66, 334-337 (1947). 



"2 H. Kaunitz and C. A. Slanetz, /. Nutrition, 36, 331-338 (1948). 



2" R. J. Blandau, H. Kaunitz, and C. A. Slanetz, /. Nutrition, 38, 97-104 (1949). 



"•• P. Suomalainen, Nature, 165, 364 (1950). 



"5 A. M. Pappenheimer and M. Goettsch, Proc. Soc. Exptl. Biol. Med., 47, 268-270 

 (1941). 



