hen a group of sheep were fed 1 gramme of copper sulphate daily there was no demonstrable effect on their blood copper levels. Three out of six may have shown a premonitary sign of poisoning in a form of photosensitisation. It was sixteen weeks before one died with the typical signs and. 'nost-mortem findings of copper poisoning, but this was followed by another in two weeks. Blood analyses indicated that there was a considerable rise of loosely- bound copper in the plasma in the terminal crisis.
When two of the survivors were given 54 mg. molybdenum daily by mouth, their blood copper level rose while that of controls remained t7-! same. This increase was accounted for mainly in the plasma fraction but, in contrast to the findings in the haemolytic crisis
of copper poisoning, the proportions of globulin-bound and loosely-bound copper remained approximately the same. The animals were not clinically affected and at the end of the period there was some evidence that their liver copper had been reduced. The distribution of copper within the liver was found to be different, in animals which had not died from copper poisoning, from that in animals which had.
In a further experiment, five sheep were kept on a constant diet and their intake and output of copper was measured. 54 mg. molybdenum per day, given by mouth, was found to raise serum copper levels, depress urine copper and raise faecal copper output. The effect of 2.0 g. sulphate per day was to enhance these effects, but sulphate alone did not produce the same results. Post-mortem examination of the kidneys of two of these animals revealed tubular reabsorption of copper and damage to tubular epitheluim.