Page 499 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

466 SECTION | V Metals and Micronutrients

VetBooks.ir ruminal reduction to sulfide could potentially result in Gooneratne, S.R., Buckley, W.T., Christensen, D.A., 1989. Review of
copper deficiency and metabolism in ruminants. Can. J. Anim. Sci.
greater thiomolybdate concentrations and worsen the clini-
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cal disease. With rapid clearance from the body, removal
from the high Mo source will quickly remove excess Mo Gould, L., Kendall, N.R., 2011. Role of the rumen in copper and thiomo-
lybdate absorption. Nutr. Res. Rev. 24, 176 182.
from the body. However, permanent damage may be pres-
Grace, N.D., Suttle, N.F., 1979. Some effects of sulfur intake on molyb-
ent that results in sustained animal deaths for weeks to
denum metabolism in sheep. Br. J. Nutr. 41, 125 136.
several months’ postexposure (Swan et al., 1998).
Howell, J.M., Gooneratne, S.R., 1987. The pathology of copper toxicity
Supplementation of copper in Mo-poisoned animals must
in animals. In: Howell, J.M., Gawthorne, J.M. (Eds.), Copper in
be done with care, especially in sheep, to prevent exces- Animals and Man. CRC Press, Boca Raton, FL, pp. 53 78.
sive copper accumulation and subsequent copper toxicosis. IMOA (International Molybdenum Association), 2006. Available at
,http://www.imoa.info..
Johnson, J.L., 1997. Molybdenum. In: O’Dell, B.L., Sunde, R.A. (Eds.),
CONCLUDING REMARKS Handbook of Nutritionally Essential Mineral Elements. Marcel
AND FUTURE DIRECTIONS Dekker, New York, pp. 413 438.
Johnson, J.L., Hainline, B.E., Rajagopalan, K.V., 1980. Characterization
The known mechanisms of Mo poisoning are a complex of the molybdenum cofactor of sulfite oxidase, xanthine oxidase,
interaction with sulfur and copper that differ significantly and nitrate reductase. J. Biol. Chem. 255, 1783 1786.
across animal species. However, some clinical effects of Kelleher, C.A., Ivan, M., Lamand, M., et al., 1983. The absorption of
Mo poisoning have not been related to absolute or func- labeled molybdenum compounds in sheep fitted with re-entrant can-
tional copper deficits, as replenishment of copper does nulae in the ascending duodenum. J. Comp. Pathol. 93, 83 92.
not result in cessation of clinical effects. Some of the King, K.A., Leleux, J., Mulhern, B.M., 1984. Molybdenum and copper
levels in white-tailed deer near uranium mines in Texas. J. Wildlife
copper-refractory clinical effects could be simply a direct
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inhibition of functional enzymes by thiomolybdates.
Ladefoged, O., Sturup, S., 1995. Copper deficiency in cattle, sheep, and
These refractory clinical effects of Mo poisoning need
horses caused by excess molybdenum. Vet. Hum. Tocicol. 37, 63.
further investigation to delineate the exact mechanism by
Lesperance, A.L., Bohman, V.R., Oldfield, J.E., 1985. Interactions of
which Mo produces adverse animal health. molybdenum, sulfate, and alfalfa in the bovine. J. Anim. Sci. 60,
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Mason, J., Cardin, C.J., 1977. The competition of molybdate and sulfate
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