Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

Although the syndrome described for bull terriers is similar
to cattle with Adema disease and humans with AE, two
significant differences should be noted. Serum Zn is not
consistently low in affected pups, and the syndrome is not
responsive to Zn therapy. These observations suggest that
the genetic lesion in Zn metabolism in bull terriers is quite
different from that in previously described disorders.
Chondrodysplasia (short-limbed dwarfism) in Alaskan
malamutes causes several deformities, but it is not life
threatening. Malamutes have been reported to have a
decreased ability to absorb Zn from the gastrointestinal
tract ( Brown et al. , 1978 ). Mutant dogs have severe bowing
of the forelimbs with gross changes in size and shape of the
humerus, radius, and ulna. There is no difference between
dwarf and normal dogs in mineral content of the long
bones and forelimbs, but in some regions calcium is more
soluble than normal. In addition to the apparent abnormality
of calcium binding, the dwarfs have high levels of urinary
acid mucopolysaccharides, suggesting a disturbance
in normal bone maturation. Dogs with this genetic lesion
can also have hemolytic anemia. In anemic dwarfs, red
cells are macrocytic, hypochromic, and without reticulocytosis.
Erythrocytes are fragile and have higher than normal
intracellular cadmium and potassium and lower than
normal glutathione. The specific defect that predisposes
the cells to premature destruction is not known.
F . Zinc Toxicity
The risk for Zn toxicity and the likelihood of achieving
excessive dietary intakes of Zn are both low. Zn has been
characterized as a relatively nontoxic element with a wide
margin of safety. However, given the diversity of enzymes