− | The nutritional essentiality of selenium was first demonstrated when it was found to be an '''integral part of the enzyme glutathione peroxidase, which protects the body against oxidative damage such as that caused by free radicals'''. In this respect selenium is closely linked with vitamin E and one nutrient can to some extent “spare” a deficiency of the other. Nevertheless, selenium has its own unique function and is a component of other enzymes and proteins. | + | The nutritional essentiality of selenium was first demonstrated when it was found to be an '''integral part of the enzyme glutathione peroxidase, which protects the body against oxidative damage such as that caused by free radicals'''. In this respect selenium is closely linked with [[Vitamin E (α-Tocopherol) - Nutrition|vitamin E]] and one nutrient can to some extent “spare” a deficiency of the other. Nevertheless, selenium has its own unique function and is a component of other enzymes and proteins. |
− | There is little direct information on the metabolism of selenium in dogs and cats but studies in other mammals, including man, show that after absorption selenium is taken up by red blood cells then released into the plasma where it is bound to albumin and transported to the tissues. In all the selenium-containing enzymes selenium exists as selenocysteine, which can be formed from selenomethionine by the same metabolic pathways that convert [[Methionine and Cysteine - Nutrition|methionine to cysteine]]. Selenium is a component of deiodinase enzymes responsible for the conversion of thyroxine to tri-iodothyronine, the active form of [[Iodine - Nutrition|thyroid hormone]]. Selenium-containing proteins have been reported to support the immune response and '''protect against certain cancers'''. There is also some evidence that selenium may be protective against the adverse effects of mercury in cats, perhaps by inhibiting its absorption<ref>Houpt, K, Essick, L, Shaw, E, Alo, D, Gilmartin, J, Gutenmann, W, Littman, C, Lisk, D (1988). “A tuna fish diet influences cat behaviour”. J. Toxicol. Environ. Health 24:161-172.</ref>. Urine is the primary excretion route for selenium and the major urinary metabolite is selenosugar B, a compound of selenium and galactosamine<ref>Suzuki, K (2005). “Metabolomics of selenium: Se metabolites based on speciation studies”. J. Health Sci. 51:107-114.</ref>. | + | There is little direct information on the metabolism of selenium in dogs and cats but studies in other mammals, including man, show that after absorption selenium is taken up by [[Erythrocytes|red blood cells]] then released into the plasma where it is bound to [[albumin]] and transported to the tissues. In all the selenium-containing enzymes selenium exists as selenocysteine, which can be formed from selenomethionine by the same metabolic pathways that convert [[Methionine and Cysteine - Nutrition|methionine to cysteine]]. Selenium is a component of deiodinase enzymes responsible for the conversion of thyroxine to tri-iodothyronine, the active form of [[Iodine - Nutrition|thyroid hormone]]. Selenium-containing proteins have been reported to support the immune response and '''protect against certain cancers'''. There is also some evidence that selenium may be protective against the adverse effects of mercury in cats, perhaps by inhibiting its absorption<ref>Houpt, K, Essick, L, Shaw, E, Alo, D, Gilmartin, J, Gutenmann, W, Littman, C, Lisk, D (1988). “A tuna fish diet influences cat behaviour”. J. Toxicol. Environ. Health 24:161-172.</ref>. Urine is the primary excretion route for selenium and the major urinary metabolite is selenosugar B, a compound of selenium and galactosamine<ref>Suzuki, K (2005). “Metabolomics of selenium: Se metabolites based on speciation studies”. J. Health Sci. 51:107-114.</ref>. |
− | Researchers of selenium deficiency in dogs have reported clinical signs and changes in selenium status. Nevertheless, despite the role of selenium in the deiodinase enzymes, selenium deficiency did not appear to be linked to hypothyroidism in dogs<ref>Wedekind, KJ, Kirk, CA, Nachreiner, RF, Yu, S (2001). “Effect of varying selenium (Se) intake on thyroid hormone metabolism in dogs”. FASEB J. 15:A953.</ref>. | + | Researchers of selenium deficiency in dogs have reported clinical signs and changes in selenium status. Nevertheless, despite the role of selenium in the deiodinase enzymes, selenium deficiency did not appear to be linked to [[hypothyroidism]] in dogs<ref>Wedekind, KJ, Kirk, CA, Nachreiner, RF, Yu, S (2001). “Effect of varying selenium (Se) intake on thyroid hormone metabolism in dogs”. FASEB J. 15:A953.</ref>. |
| #'''Selenium depletion''': Puppies fed a diet deficient in vitamin E and selenium, (selenium content 0.01 mg/kg on a dry matter (DM) basis) developed various clinical signs including anorexia, depression, abnormal breathing and coma within 6-8 weeks. Post mortem examination revealed muscular degeneration and renal mineralisation. Even when puppies were supplemented with selenium (dietary content of 0.5 mg/kg DM), mild skeletal myopathy was observed<ref>. Van Vleet, J, (1975). “Experimentally induced vitamin E-selenium deficiency in the growing dog”. J. Am. Vet. Med. Assoc. 166:769-774.</ref>. | | #'''Selenium depletion''': Puppies fed a diet deficient in vitamin E and selenium, (selenium content 0.01 mg/kg on a dry matter (DM) basis) developed various clinical signs including anorexia, depression, abnormal breathing and coma within 6-8 weeks. Post mortem examination revealed muscular degeneration and renal mineralisation. Even when puppies were supplemented with selenium (dietary content of 0.5 mg/kg DM), mild skeletal myopathy was observed<ref>. Van Vleet, J, (1975). “Experimentally induced vitamin E-selenium deficiency in the growing dog”. J. Am. Vet. Med. Assoc. 166:769-774.</ref>. |