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There is evidence from animal experiments that the requirements for certain of the vitamins are increased by pregnancy. However, there is little precise information with respect to changes during pregnancy and lactation in women's needs for vitamins. The recent development of reliable methods for determining the amount of vitamin C in tissues and in biologic fluids has offered opportunity for studies during human pregnancy and lactation. A number of observations have appeared in the literature of the past three years concerning the ascorbic acid content of maternal blood, of fetal blood and of the placenta, although no one seems to have followed a series of pregnant women consistently through pregnancy and delivery to obtain related and comparative values.Neuweiler,1 using Gabbe's technic with modifications, reported a higher content of ascorbic acid in blood from the umbilical vein than in that from the umbilical artery (1.9 to 3.6 versus 0.7 to 2.1 mg. per hundred cubic centimeters). On the basis of this observation and of earlier work in which he found a considerable amount of ascorbic acid in the placenta, Neuweiler -could not accept the claim of Rohmer and Bezssonoff 3 that the human fetus can synthesize ascorbic acid. Abt, Farmer and Epstein,4 using indophenol blue titration of a tungstic acid filtrate, reported identical values for the reduced ascorbic acid of From the

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The effect of the specific muscle toxicant, 2,3,5,6-tetramethyl p-phenylenediamine (TMPD), on urinary creatine and taurine, markers of testicular and liver dysfunction, respectively, has been investigated in male Sprague-Dawley rats. Damage to the gastrocnemius and soleus muscles was accompanied by a rise in serum creatine kinase (predominantly the muscle-specific isoenzyme, CK-MM), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Increases in serum alpha-hydroxybutyrate dehydrogenase (HBDH) and total lactate dehydrogenase (LDH) (mainly isoenzymes, LDH1 and LDH2), occurred but only minor damage to the heart and no rise in CK-MB, (heart muscle isoenzyme) was seen. Damage to stage XIV tubules in the testis was evident histologically after the highest dose. This was accompanied by an increase in LDH-C4 testis-specific isoenzyme and a decrease in serum testosterone. Apart from reduced serum albumin, no other serum parameters indicated liver damage and there was only slight liver steatosis in some animals at the highest dose. Urinary taurine was not significantly raised after any dose of TMPD, but there was a significant increase in urinary creatine after the highest dose. It can be concluded that in the presence of discrete muscle damage, the use of urinary taurine and urinary creatine as markers of liver and testicular dysfunction, respectively, is not confounded. However, a variety of different markers should be used in conjunction to fully delineate the tissue damage due to toxic chemicals.