Blood Cell Transaminase Activity in Human Vitamin B6 Deficiency

phate has been well established in trans-aminase enzyme systems. Studies in rats have shown that in vitamin B, deficiency, blood transaminase activities are greatly depressed and respond to in vitro addition of pynidoxal phosphate or in vivo administration of vitamin B,. This response is illustrated by the reports of Brin et a!., ‘ Babcock2 and others. The re-sponse in blood transaminase activities in human vitamin B, deficiency has not been as great. Babcock et al.3 concluded from studies with human subjects on a diet low in vitamin B6 that because of the wide normal range of transaminase activity, a single determination, even at the height of deficiency, was not suffi-cient to assess the degree of deficiency. They thought that the increase in transaminase ac-tivity on repletion with 5 to 10 mg. of vitamin B6 per day was more indicative of deficiency. Previous data from this laboratory4 have also demonstrated a slight but nonsignificant (P> 0.05) decrease in serum glutamic oxaloacetic transaminase activity in human subjects fed a vitamin B,.deficient formula diet for three weeks. The serum glutamic oxaloacetic trans-aminase activity did not rise to predeficiency levels even after supplementation with 10 mg. pyridoxine per day for three weeks. Cheslock and McCully, ’ on the other hand, have shown in adults on a diet supplying 0.4 mg. vitamin B, per day (comparable to the intake by the sub-jects of Babcock) that blood vitamin B, was not detectable after four weeks. Ranke et al.’ found in aged human subjects (seventy-tw