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1. Increasing concentrations of cobalt in the medium result in increased production of an iron-binding compound and a corresponding fall in catalase activity of Neurospora crassa. 2. Cobalt rapidly depletes the medium of iron by enhancing the rate of iron uptake by the mycelium. 3. With toxic amounts of cobalt there is a fall in bound 59 Fe and haem 59 Fe as well as a decreased incorporation of [2- 14 C]glycine into the mycelial haem fraction. The production of the iron-binding compound precedes the fall in the iron-dependent systems mentioned. 4. The 59 Fe bound to the iron-binding compound acts as a better iron source for haem synthesis in cell-free extracts as compared with 59 FeSO 4 . 5. Cobalt inhibits iron incorporation into protoporphyrin in cell-free extracts but is not itself incorporated to an appreciable extent.

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INDEPENDENT investigation here and in the United States led to the recent isolation of the anti-pernicious anaemia factor as red needle-shaped crystals1–3. Examination of its ash has now unexpectedly revealed the presence of cobalt.

1. 1.A study using Neurospora crassa was made of the effects of Fe deficiency and toxicities of Mn, Zn, Cu, Mo, Co, and Ni on the enzymes: cytochrome oxidase, catalase, peroxidase, and succinic dehy-drogenase; those of iron deficiency and cobalt toxicity on nitrate reductase, “glucose 6-phosphate dehydrogenase,” isocitric dehydrogenase, DPNase, and alkaline phosphatase. 2. 2. A striking similarity was noted between iron deficiency and cobalt toxicity, not only on the activity of the iron enzymes but also on the activity of other enzymes not known to involve iron directly. It is suggested that iron deficiency and cobalt toxicity produce similar effects on the over-all metabolism of this organism. 3. 3.Some form of direct competition between iron and cobalt may be responsible for some of these effects, and possible implications are discussed.

The natural history of a new disease entity in chronic beer drinkers consisting of pericardial effusion, a low cardiac output, and in about half of the cases of polycythemia is presented. Normalization of the heart volume, the hemoglobin value, and the hemodynamic state was obtained in patients who stopped drinking. Further evidence of the importance of cobalt in the development of the disease is presented. All patients drank beer to which cobalt was added and the disease was not seen in chronic alcoholics drinking wine or other alcoholic beverages. In view of the rather small quantity of cobalt consumed, an hypothesis is formulated which attributes the cobalt toxicity in chronic alcoholics, to a dietary deficiency of sulfhydryl-groups containing amino acids and a dietary deficiency of protein.

Cobalt has been demonstrated to be effective in the treatment of certain anemias.1In combination with iron, it is of value in the treatment of anemia of prematurity and infancy.2Cobalt and iron have been found to be effective in the prevention and treatment of most pregnancy anemias.3In this article, it was stated that no toxic manifestations from cobalt therapy had been observed in pregnant women or their offspring. Because of current interest in cobalt toxicity, specifically, the possibility of cobalt inducing thyroid hyperplasia and hypothyroidism4complete investigations in animals and pregnant women are to be reported. METHOD Observations on 78 pregnant women have been completed; 58 received cobalt and iron, and 20 received cobalt alone. The iron and cobalt preparation given to the first group provided 60 to 90 mg. of cobaltous chloride with iron per day. The second group received 75 to 100 mg.