Vitamin B12 and hemoglobin regeneration in the chick.

At the time that the isolation of crystalline vitamin B,z was announced (l), it was reported that this vitamin was extremely effective in the treatment of Addisonian pernicious anemia (2). These and other reports (3, 4) indicated that, in the human, vitamin Blz apparently stimulates the bone marrow to produce mature erythrocytes and myeloid leucocytes. In baby pigs, vitamin Blz was found by Neumann et al. (5) to promote erythropoiesis, but not to an optimum level, judging by an abnormally high erythroid percentage in the bone marrow. These authors also reported (6) that a deficiency of vitamin B1z in the diet of the baby pig did not affect the hemoglobin level or red blood cell count, but did affect the bone marrow to the extent that the percentage of neutrophiles was greatly increased: 84 per cent in vitamin Blz-deficient animals and 20 and 14 per cent in supplemented animals. In the fox (7) and in the mink (8), a deficiency of an unknown factor, possibly vitamin B,z, resulted in severe anemia and other deficiency symptoms. Zucker and Zucker (9) observed that rats deficient in zoopherin (vitamin Blz) suffered high mortality in the post-weaning period, possibly from gastric hemorrhage. These workers also noted that the average leucocyte count was lower during the 2 weeks after weaning than either before or after this period. Further investigations regarding hematology of the vitamin Blz-deficient rat were made by Borson et al. (lo), who reported that the most striking sign of vitamin B1, deficiency which results in the death of the rat was the reduced leucocyte count. Nursing pups with leucocyte counts of 5000 per c.mm. or above tended to survive, whereas those with counts of 3000 per c.mm. or less died without exception. The granulocyte counts were closely correlated with the total leucocyte count, but the hemoglobin level was not so closely related. The authors suggest that the leucopenia does not itself cause death, but is a reflection of the