Selenium - Nutrition

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What is Selenium?

Selenium is a trace element that, like iodine, is required in only very small quantities. Chemically it is classified as a semi-metal or metalloid element and can exist in four oxidation states: 2-, 0, 4+ and 6+. This accounts for its existence in several different forms in nature, e.g. as 4+ in sodium selenite (Na2SeO3), 6+ in sodium selenate (Na2SeO4) and 2- in selenocysteine.

Why is it Important?

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.

Roles in the Body

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 to cysteine. Selenium is a component of deiodinase enzymes responsible for the conversion of thyroxine to tri-iodothyronine, the active form of 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[1]. Urine is the primary excretion route for selenium and the major urinary metabolite is selenosugar B, a compound of selenium and galactosamine[2].

Consequences of Selenium Deficiency

Dog:

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[3].

Recognised Syndromes Related to Selenium Deficiency

  1. 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[4].
  2. Serum selenium: Purified diets containing a selenium content of less than 0.21 mg/kg DM were insufficient to support normal serum selenium concentrations in 9-week-old beagle puppies[5].

Cat:

Studies on selenium deficiency in cats have concentrated on indicators of selenium status.

Recognised Syndromes Related to Selenium Deficiency

  1. Serum glutathione peroxidase depletion: Ten-week-old kittens fed diets with a selenium content of less than 0.12 mg/kg DM did not maintain normal glutathione peroxidase activity[5][6]. In another study, kittens receiving a very low dietary selenium content of 0.02 mg/kg DM showed reduced plasma selenium and glutathione peroxidase activity compared with a control group receiving a diet containing a selenium content of 0.4 mg/kg DM[7].
  2. Thyroid hormones: In the same study[7], the selenium deficient diet also caused an increase in plasma thyroxine and a decrease in tri-iodothyronine but the values did not fall outside the normal ranges. This is similar to the result in dogs in that selenium is linked to the metabolism of the thyroid hormones but a deficiency does not appear to cause overt signs of hypothyroidism.

Toxicity

Dog:

Selenium is probably the only nutrient that was studied for its toxic effects many years before its essentiality was discovered. A study in 1943[8] showed that dietary selenium contents of 10 mg/kg DM as sodium selenite or 7.2 mg/kg DM as organic selenium were toxic to dogs as indicated by impaired growth and low food intake. More recent investigations showed that when dogs were fed a dietary selenium content of 5 mg/kg DM for 24 weeks resulted in both a reduction in food intake and impaired hair growth[9][10].

Cat:

Cats seem to be more resistant than dogs to the toxic effects of selenium. Adult cats were fed up to 10 mg selenium/kg diet DM in an organic form (selenomethionine) for 26 weeks with no signs of toxicity[11]. The difference in selenium tolerance between the two species can be explained by the fact that cats are more efficient at excreting excess selenium in the urine and store less selenium in the liver[12].

Dietary Sources

Selenium is found in a wide variety of plant and animal sources but usually at low concentrations. Meats, fish and bread are reported to supply good amounts of bioavailable selenium. Some studies suggest that plant sources are more bioavailable than animal sources. In commercial pet foods, selenium bioavailabilities of 30% and 53% for canned and dry products, respectively have been reported[13]. To ensure nutritional adequacy pet foods can be supplemented with inorganic selenium compounds such as sodium selenate or selenite or an organic source like selenomethionine. The bioavailabilities of these selenium compounds appear to be similar: a study comparing high intakes of selenium in cats and dogs fed selenium in either inorganic or organic forms found no major differences in results for the two sources[12].

References

  1. 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.
  2. Suzuki, K (2005). “Metabolomics of selenium: Se metabolites based on speciation studies”. J. Health Sci. 51:107-114.
  3. 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.
  4. . Van Vleet, J, (1975). “Experimentally induced vitamin E-selenium deficiency in the growing dog”. J. Am. Vet. Med. Assoc. 166:769-774.
  5. 5.0 5.1 Wedekind, KJ, Combs Jr, GF (2000). “Selenium in petfoods: Is bioavailability an issue?”. Compend. Contin. Educ. Pract. Vet. 22(suppl.):17-22.
  6. Wedekind, KJ, Howard, K, Backus, R, Rogers, QR (2000). “Current AAFCO and NRC recommendations for selenium (Se) are too low for kittens”. FASEB J. 14:A295.
  7. 7.0 7.1 Yu, S, Howard, K, Wedekind, KJ, Morris, JG, Rogers, QR (2001). “A low-selenium diet increases thyroxine and decreases 3,5,3’-tri-iodothyronine in the plasma of kittens”. J Am. Physio. Anim. Nutr. 86:36-41.
  8. Rhian, M, Moxon, AA (1943). “Chronic selenium poisoning in dogs and its prevention by arsenic”. J. Pharm. Exp. Therap. 78:249-264.
  9. Wedekind, KJ, Kirk, CA, Yu, S, Nachreiner, RF (2002). “Defining the safe lower and upper limits for selenium (Se) in adult dogs”. Fed. Proc. 16:A992-A993.
  10. Yu, S, Wedekind, KJ, Kirk, CA, Nachreiner, RF (2006). “Primary hair growth in dogs depends on dietary selenium concentrations”. J. Anim. Physiol. Anim. Nutr. 90:146-151.
  11. Wedekind, KJ, Kirk, CA, Yu, S, Nachreiner, RF (2003). “Defining the safe lower and upper limits for selenium in adult cats”. J. Anim. Sci. 81(suppl.):90 (abstr.).
  12. 12.0 12.1 Todd, SE, Thomas, DG, Bosch, G, Hendriks, WH (2012). “Selenium status in adult cats and dogs fed high levels of dietary inorganic and organic selenium”. J. Anim. Sci. 90:2549-2555.
  13. Wedekind, KJ, Beyer, R, Combs Jr, GF (1998). “Is selenium addition necessary in petfoods?”. FASEB J. 12:A823.



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