Chemistry Reference
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(Deosthale and Gopalan, 1974), but this effect was not
observed in a controlled study with high dietary molyb-
denum (Turnlund and Keyes, 2000).
Copper toxicity has been treated with tetrahydro-
molybdate in humans and a number of other species.
Wilson's disease, an autosomal recessive disorder
of copper storage in humans, is associated with cop-
per accumulation in the liver and brain resulting in
neurological damage and cirrhosis. Penicillamine is
often used to remove excess copper. An alternative
treatment is the administration of tetrahydrothiomo-
lybdate (Brewer and Yuzbasiyan-Gurkan, 1992; Turn-
lund, 2002). After administration of terathiomolybdate,
plasma copper levels rise and copper is excreted in the
urine. LEC rats have a disorder resulting in accumula-
tion of copper in the liver similar to Wilson's disease.
Administration of tetrathiomolybdate mobilizes copper
from the liver complexed with tetrathiomolybdate.
Molybdenum and copper are then excreted in equimo-
lar amounts into the bile (Komatsu et al ., 2000). Ammo-
nium tetrahydromolybdate has been considered the
treatment of choice for copper toxicity in sheep. Recent
studies demonstrated that pituitary endocrinopathy
and cessation of reproductive activity were observed
with this treatment, raising concern about the practice
(Haywood et al ., 2004).
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