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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.

All chambers of the heart are affected in experimental cobalt cardiomyopathy, with atrial predilection. The primary morphological alteration is mitochondrial damage that possibly reflects an enzymatic block of oxidative decarboxylation at pyruvate and ketogluterate levels. In acute cobalt toxicity chelation of calcium may also be a contributory factor, resulting in deficient utilization of high-energy phosphates. Experimental cobalt cardiomyopathy requires preconditioning factors: protein deficiency appears to be one of them. Vegetative polypoid endocarditis is an important accompaniment in the model used, suggesting that in rats on a protein deficient diet cobalt produced endothelial damage in addition to a cardiocyte injury. [ABSTRACT FROM PUBLISHER]

Indwelling electrodes were implanted in rats one week before intraperitoneal injections of cardiotoxic doses of cobalt. Electrocardiograms were recorded from the rats at varying time intervals after dosing. The rats were subsequently killed and their hearts were examined histologically. The topography and histological characteristics of the cardiac lesion were established and were compared with alterations in the electrocardiogram. [ABSTRACT FROM PUBLISHER]