Copper deficiency symptoms are caused by thiomolybdate and not by low blood copper levels.
It has long been known that molybdenum is involved in copper deficiency but it is now becoming clear that, when combined with sulphur, it actually causes the symptoms which we call copper deficiency.
When molybdenum and sulphur are present in the rumen the bacteria combine them to form thiomolybdates (MoSn). These compounds must combine with copper and once they have done so the copper present in copper-thiomolybdate is no longer available to the animal.
If thiomolybdate does not find copper in the rumen it passes through into the blood and tissues where it seeks out the most available forms of copper and in attaching to it makes it unavailable to the animal. Once it has taken out all of the amino acid copper present in the plasma it next comes to the copper metallo-enzymes and when it extracts the copper from these it stops them from working. The animal continues to produce the enzymes but as quickly as it does so thiomolybdate moves in to deactivate them. It is this deactivation of copper enzymes that causes the clinical symptoms of copper deficiency not the lack of copper. So even when an animal has adequate levels of total copper it can still show symptoms, which we know as copper deficiency, including infertility, poor coat, and (in sheep and deer) swayback.
The only way to stop thiomolybdate from deactivating vital enzymes is to provide a more available form of copper before it reaches them, and the best place to do this is before the thiomolybdate enters the blood i.e. in the rumen.