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

V. Molybdenum
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FIGURE 22-5 Molybdenum cofactor. Mo as molybdates enter cells by way of oxyanion transporters. A series
of complex condensation and reductive steps (e.g., formation of the pterin precursor from guanidine triphosphate
[GTP] and condensation with molybdenum) result in the formation of the molybdenum cofactor. The cofactor is
essential for the activities of sulfite oxidase, xanthine dehydrogenase, and aldehyde oxidase (see text).
The clinical signs of molybdenosis also include lameness;
weight loss; anorexia; loss of color and quality of the wool
or hair; and in cattle, diarrhea. Thiomolybdates are used to
treat chronic Cu toxicosis, to help mobilize stored Cu and
reduce the high oxidizing of free Cu ( Brewer et al. , 2006 ;
Spears, 2003 ; Suttle, 1991 ).
D . Other Disorders
In human animals, combined deficiencies of xanthine dehydrogenase/oxidase
and sulfite oxidase have been reported
in humans. The cause of the decreased enzyme activities
is thought to be the loss of Mo cofactor that results in
a functional Mo deficiency. Single enzyme deficiencies of
xanthine dehydrogenase/oxidase and sulfite oxidase have
also been described ( Mendel and Bittner, 2006 ; Schartz,
2005) . Xanthinuria and elevated serum uric acid have been
reported in patients with xanthine dehydrogenase deficiency.
A severely debilitating condition in children is sulfite oxidase
deficiency that leads to severe aberrations in sulfur and
sulfur amino acid metabolism ( Mendel and Bittner, 2006 ;
Schartz, 2005) .