Readers' Rating:

Rate this article

Send to a friend

Selenium has been reported to be an essential nutrient for both cats and dogs (National Research Council, 1985; 1986) although there have been no deficiency studies in cats. In dogs, muscular weakness, subcutaneous oedema, anorexia, depression, dyspnea and eventual coma were reported in association with selenium deficiency by Van Vleet (1975) who also observed signs of muscular degeneration, necrosis in the myocardium and renal mineralisation in selenium-deficient dogs. Manktelow (1963) and Van Rensburg and Venning (1979) reported similar lesions in growing and adult dogs made selenium-deficient.

Domestic cats and dogs both belong to the order Carnivora. The cat is regarded as a true carnivore while the dog is often described as an omnivorous carnivore. Cats have many metabolic adaptations which result from their carnivorous dietary habit throughout evolution (MacDonald and Rogers, 1984; Morris, 2002). All the identified metabolic adaptations are consistent with the consumption of diets containing a very constant amount of a particular nutrient (e.g. - vitamin A, D, niacin) or a total absence of a nutrient (e.g. - carotene) compared to omnivores. Dogs show two metabolic adaptations believed to result from their carnivorous diets: a lack of vitamin D synthesis and a relatively low rate of arginine synthesis.

Although the metabolic adaptations of cats and dogs are well known (an excellent review has been published by Morris, 2002), the importance of the highly specialised dietary requirements of cats and the differences compared to omnivorous animals is often underestimated (Zoran, 2002). However, there seems to be a growing realisation of the importance of the ‘carnivore connection’ of cats and dogs, although this realisation is stronger for the former. The following contribution will discuss the selenium intake of cats and dogs based on modern pet foods in relation to selenium levels and forms in diets throughout evolution.

In order to determine the main sources of selenium intake in cats and dogs an understanding of their diets throughout evolution is required as well as the forms of selenium present in their diets.


Evolution of cats and dogs

The domestic dog and cat both belong to the order Carnivora, meaning ‘meat eaters’. However, many species within the order Carnivora are far from being meat-eaters. The giant panda (Ailuropoda melanoleuca) consumes a diet predominantly consisting of bamboo, while brown bears (Ursus arctos) rely on a diet containing animal as well as plant material such as grasses, sedges, roots, moss, bulbs, fruits, nuts and berries (Wilson and Ruff, 1999).

It is believed that the cat has evolved a number of metabolic adaptations (compared to omnivores such as the rat and pig) as a result of a consistent intake of nutrients originating almost exclusively from animal tissues with little ingestion of plant-based materials. Although the latter cannot be proven, all the cat’s morphological, anatomical, physiological and metabolic adaptations lead to the conclusion that the cat is an obligatory carnivore. Additional evidence can be found in the taste system of the cat, which is responsive to amino acids, dipeptides, lipids, nucleotides, carnosine, etc (Boudreau and White, 1978) but not sugars such as sucrose, fructose and glucose (Beauchamp et al., 1977).

The modern day wild cats maintain an obligatory carnivorous diet and are very opportunistic feeders, consuming predominantly rodents, birds and insects (Fitzgerald and Karl, 1979; Jones and Coman, 1981). The present-day breeds of domestic cats (100+ breeds) are believed to be descendants of the European wild cat (Felis silvestris) and the African wild cat (Felis libyca) (Clutton-Brock, 1981; MacDonald and Rogers, 1984).

The general consensus is that domestic dogs (Canis familiaris) are omnivorous carnivores as they show adaptations (morphologic, anatomic, physiologic, and metabolic) towards the ingestion of meat as well as some plant material (Morris and Rogers, 1989; Hendriks and Moughan, 2000). The morphometric dimensions of the gastrointestinal tract and the dental anatomy clearly point to a carnivorous diet although the presence of crushing molars, which are normally associated with the capacity to ingest plant material, suggests an omnivorous diet (Morris and Rogers, 1989; Maskell and Johnson, 1993). In terms of metabolic adaptation, modern day dogs show two adaptations consistent with a carnivorous diet similar to those of cats: a lack of vitamin D synthesis and a reduced ability to synthesise arginine. The alleged ‘omnivore connection to nutrition in dogs’, as pointed out by many nutritionists, is difficult to place in the context of this species’ evolution.

The possibility that dogs (or their ancestors) would have ingested significant quantities of plant-based materials such as grasses, grains, roots, bark, berries, bulbs, nuts or fruits is difficult to envisage.

The dog was one of the earliest animals domesticated by humans (around 10,000 BC). The wolf (Canis lupus) is generally regarded as the common ancestor of the approximately 150+ dog breeds that exist today (Mech, 1970; Röhrs, 1987). Wolves normally hunt in packs of around 15 to 20 animals and a pack normally hunts relatively large prey. The dietary intake of wolves in the wild has been characterised extensively and mainly consists of larger animals like deer, elk, bison, hares, moose, caribou, elk, sheep, goats and beavers (Mech, 1970) although smaller animals have also been reported to be in the wolf’s diet (Röhrs, 1987). A pack of wolves leaves little remaining of their prey, consuming all but the bone and hair (Mech, 1970). Röhrs (1987) also reports that dogs consume berries, apples, pears, bush cherries, fungi and melons but these food items are a minor component of the normal diet of wolves. The large stomach volume of wolves assists in consuming and storing food for extended periods of time. In addition to the animal tissue consumed by wolves, the digestive tract (including content) of the prey is also consumed providing evidence of the ‘omnivorous connection’ of dogs to what otherwise would be classified as a nearly true carnivore.


Forms of dietary selenium

The forms of selenium ingested by animals can be grouped into inorganic and organic categories. Inorganic selenium exists as minerals in the form of selenite, selenate and selenide, as well as the metallic form. The primary organic forms of selenium include selenomethionine and selenocysteine.

Plants absorb inorganic selenium from the soil in the form of selenite or selenate and synthesise organic selenium in the form of selenoamino acids, of which selenomethionine is the main form. Se-methylselenomethionine and Se-methyl-selenocysteine are also found in plants. The ability of plants to obtain selenium depends on its concentration in the soil, which is variable, as well as soil pH and aeration (Surai, 2002). Thus selenium concentration in the plant component of ingredients for animal feeds may vary considerably. Animals obtain dietary selenium from cereals and grains, or from the tissues of other animals, depending on dietary habit. Selenomethionine cannot be synthesised by animals and must be obtained from the diet.

The forms of dietary selenium from both plant and animal sources include a range of inorganic and organic selenium compounds. The primary form of selenium in plants is selenomethionine, together with smaller amounts of selenocysteine and selenite. The forms of selenium found in animals include selenoproteins (formed from biologically active selenocysteine, e.g. – glutathione peroxidase, selenoprotein P), Se-containing proteins (formed from non-specific incorporation of selenomethionine or selenocysteine) as well as nonprotein and inorganic selenium (selenite, selenate) and methylated selenium (forms that are excreted) (Lobinski et al., 2000).


Selenium metabolism

Selenium metabolism in humans and livestock has been reviewed by many authors, however whether all the metabolic pathways described for selenium are similar in cats and dogs has yet to be determined. Ruminant metabolism of selenium is somewhat different to that of monogastric species due to the presence of rumen microbes that create a reduced environment (Jacques, 2001).

Absorption of selenium is not regulated metabolically; however the amount of selenium absorbed is dependent on the chemical form, concentration in the dietary source, and other factors present in the diet that may affect bioavailability (Whanger, 1998). The mechanism by which selenium is absorbed (which is dependent on form) determines the rate of absorption. Selenite is absorbed by passive diffusion whereas selenate and organic selenium (selenomethionine and selenocysteine) are actively absorbed (Wolffram et al., 1986; 1989). Absorption of selenate, selenomethionine and selenocysteine are competitively inhibited by sulphate, methionine and cysteine, respectively (Wolffram et al., 1988; 1989). In general selenomethionine is better absorbed than selenite (Daniels, 1996). In addition the rate of selenoamino acid absorption is dependent on the rate and degree of protein digestion, gut transit time, and other factors including heat damage to protein during processing.

Absorbed selenium is transported in plasma bound to proteins where it is either used for selenoprotein synthesis, stored or excreted (Figure 1).

Biologically functional selenoproteins contain selenocysteine. In order to synthesise selenoproteins, animals must first convert dietary selenium of organic or inorganic origin to selenocysteine. This occurs through a metabolic intermediate, hydrogen selenide.

As a result, dietary selenate is reduced to selenite which is further reduced to selenide. Selenomethionine is converted to selenocysteine which in turn is degraded to selenide (Jacques, 2001) and used to form selenocysteine, which can then be incorporated into the active site of a selenoprotein. If dietary selenium of inorganic origin is not used for selenoprotein synthesis it is rapidly methylated and excreted via the lungs or kidneys. In contrast, dietary selenium of organic origin may be stored in general body proteins.

Selenomethionine and selenocysteine can be incorporated into body proteins such as muscle in place of the amino acids methionine and cysteine, respectively, as they share the same metabolic pathways. This stored selenium can be released during protein turnover. Hence selenomethionine and selenocysteine from either dietary or tissue origin provide a source of selenium for selenoprotein synthesis.

Cysteine in mammals is an intermediate for the synthesis of taurine through the intermediate cysteinesulphinic acid. It follows that any selenocysteine generated in vivo would follow a similar metabolism to cysteine and it can be expected that selenotaurine would be formed. Cats are well known for their lack of de novo taurine synthesis due to the low activity of the enzymes cysteine dioxigenase and cysteine sulphinic acid decarboxylase. The lack of taurine synthesis lies in the transamination of cysteine sulfinate, an intermediate in taurine synthesis, rather than the decarboxylation leading to taurine (Edgar et al., 1998). Any selenocysteine formed in cats will be quickly transaminated to puryvate with release of the selenium (Figure 2).





Figure 1. Overview of selenium metabolism in monogastric species (adapted from Jacques, 2001).



Selenium in the animal

Selenium occurs in all cells and tissues of the body, although concentrations vary depending on the tissue and the dietary selenium intake. In general, tissue selenium concentrations can be ranked in descending order with highest concentrations found in kidney, followed by glandular tissues (pancreas, pituitary, liver), muscle (cardiac higher than skeletal), bone, blood and adipose tissue (Underwood, 1971).

In a study by Windisch et al. (1998) the distribution of selenium in tissues was determined in rats fed selenite, selenocysteine and selenomethionine (Table 1). These results illustrate how the various forms of selenium are metabolised and utilised in different ways. Whole body selenium in rats fed organic selenium increased compared to those fed inorganic selenium. This is due to the non-specific incorporation of the organic selenoamino acids into general body proteins. The distribution of selenium in rats fed selenocysteine shifted from organs and blood towards the carcass and this was even more pronounced in rats fed selenomethionine.

Thus, greater amounts of selenium were located in muscle, skin and hair when rats were fed organic selenium compared to inorganic selenium. In their nonfunctional role, selenoamino acids accumulate in these tissues until released by protein turnover and are ‘recycled’. In contrast, any selenite not used for the synthesis of selenoproteins is excreted. Consequently, there is comparatively less selenium from selenite in tissues where high rates of protein metabolism occur compared with organic selenium, and relatively higher amounts of selenium from selenite in tissues rich in the functional selenoproteins.



Table 1. Distribution of whole body selenium among tissues in rats.


Obtained from Windisch et al. (1998)






Figure 2. Sulphur amino acid metabolism in mammals (From Morris et al., 1990).



There are several families of functional selenoproteins. These include the glutathione peroxidases, the iodothyronine deiodinases and the thioredoxin reductases. In addition there are several other selenoproteins whose functions have not yet been fully characterised including, amongst others, selenoprotein P and selenoprotein W (Holben and Smith, 1999). An outline of the function and location of selenoproteins in the body is provided in Table 2.

Selenium in blood is found in plasma and erythrocytes and in humans is estimated to comprise 3.4 and 4.3% of total body selenium, respectively (Oster et al., 1988). Two of the selenium-containing proteins in erythrocytes include glutathione peroxidase and haemoglobin. In plasma, selenium is contained in glutathione peroxidase, selenoprotein P and albumin. The distribution of selenium among these fractions is dependent on the dietary form of selenium and overall selenium status. The selenoproteins (glutathione peroxidase and selenoprotein P) contain selenocysteine, whereas the selenium-containing proteins (haemoglobin and albumin) contain selenomethionine (Whanger et al., 1994). The distribution of selenium in the plasma of rats fed selenite was: gluthathione peroxidase – 17%, selenoprotein P – 57%, albumin – 24% (Whanger et al., 1994). Similar results were obtained when the rats were fed selenomethionine. Thus selenoprotein P appears to contain the majority of selenium in the plasma of rats.


The selenium intake of the cat and dog throughout evolution

The carnivorous cat normally consumes a diet of whole prey such as rats or mice and the forms of selenium ingested include the functional selenoproteins such as glutathione peroxidase and selenoprotein P, the selenoamino acids selenomethionine and selenocysteine, as well as non-functional stored selenium that has been incorporated into body proteins such as skeletal muscle, hair and nails.

The dog in the wild would also consume selenium obtained from animal tissue, however as the wild dog would not usually eat a whole carcass at one time, the amount and form of selenium ingested would depend on the part of the animal consumed. For example the liver is a primary site of selenoprotein synthesis and contains selenoprotein P, glutathione peroxidase and other functional selenoenzymes. In contrast, the gastrointestinal tract may contain plant material that the prey animal has eaten, and therefore may contain inorganic selenite or selenate, as well as organic selenomethionine.

The primary source of dietary selenium for both cats and dogs originates from animal tissue, i.e. - the organic forms of selenomethionine and selenocysteine. The commercially prepared diets cats and dogs are fed today are somewhat different from what their ancestors would have eaten. Most of these diets contain a high proportion of plant material and for the cat as a true carnivore this may not be particularly suitable. Selenium concentrations of pet foods is highly variable (Simcock et al., 2005). In addition to selenium from the ingredients themselves, selenium may also be added to the diet. In the past, inorganic forms of selenium, primarily selenite, have been used to supplement animal feeds. Selenite was found to have a pro-oxidant effect and therefore the use of selenate was preferred. However because inorganic selenium cannot be stored in the body, organic forms of selenium are being increasingly used as they are safer and more efficiently used.



Table 2. Function and distribution of the primary selenoproteins.


^{To enlarge the image, click here
a}Holben and Smith, 1999; ^bSunde, 2000; Edens and Gowdy, 2004; ^cDaniels, 1996



The question remains as to whether selenium metabolism in carnivores differs to that in omnivores. Based on the fact that cats and dogs have several metabolic adaptations to account for their carnivorous diet, and that they evolved on diets containing primarily organic selenium, it is possible that selenium metabolism in these two species would differ from that of omnivorous animals such as pigs, poultry, rats and mice.


Selenium deficiency

Selenium deficiency in cats and dogs does not appear to be a significant problem. There are reports in the literature from the 1960s and 1970s of both naturally occurring and experimentally induced selenium deficiencies in dogs (Manktelow, 1963; Van Rensburg and Venning, 1979; Van Vleet, 1975) but there are no reports in cats. This may be due to the fact that most domestic cats and dogs today are fed commercial pet foods that typically contain adequate levels of selenium (Simcock et al., 2005), thereby preventing deficiencies.


Toxicity

Several early reports of experimentally induced selenium toxicity in dogs have been published (Anderson and Moxon, 1942; Heinrich and MacCanon, 1957; Rhian and Moxon, 1943), however there are no accounts of toxic effects of selenium in cats and there are no reports of naturally occurring toxic effects in cats or dogs. There is some evidence to suggest that cats may be able to tolerate higher levels of selenium than other species. Chronic effects of selenium toxicity in humans and livestock generally occur at around 5 ppm (Koller and Exon, 1986), however pet foods have been found to contain up to 6 ppm selenium (Mumma et al., 1986; Simcock et al., 2005). In addition, it has been reported that selenium concentrations in cat plasma are up to five times higher than in other species (Forrer et al., 1991; Foster et al., 2001). Other authors found significantly higher serum selenium concentrations in cats compared to dogs when fed selenium at 10 ppm for periods ranging from six weeks to six months (Wedekind et al., 2003; Todd et al., unpublished). Yet despite these high levels of selenium, there have been no reports of selenium toxicity.

Within the normal physiological range, selenium metabolism is controlled by urinary excretion (Levander, 1986), however at higher levels urinary excretion of selenium is less efficient (Kirchgessner et al., 1997) and it is excreted via the lungs (Sunde, 2000). Selenium metabolism in adult cats appears to be well regulated by urinary excretion at concentrations of up to 2 ppm (Todd et al., unpublished). Preliminary results from a study where cats were fed 2 ppm selenium as selenite or organic selenium yeast (Sel-Plex®) showed rapid urinary excretion of selenium. Urinary selenium excretion reflected the dietary selenium intake of both forms (Figure 3).

Thus it may be that cats and dogs are better able to tolerate higher levels of selenium than other species due to an ability to rapidly control selenium metabolism by urinary excretion.


Bioavailability of selenium in cat and dog diets

The different forms of selenium follow different metabolic paths, are utilised differently, and therefore have different bioavailabilities. Organic selenium is thought to be more bioavailable than inorganic selenium because it is stored in tissues. In addition, organic selenium has been found to maintain functional enzyme activities as well as selenium concentrations in blood and tissues for longer following selenium depletion, compared with inorganic forms (Wolffram, 1999). Thus it would seem that organic selenium is a more beneficial source of selenium, and as cats and dogs in their natural state obtained dietary selenium primarily as selenomethionine and selenocysteine in plant and animal tissue proteins, it would make sense to provide their modern domestic counterparts with the same thing.

However, there are a number of factors that can affect the bioavailability of selenium. Wedekind et al. (1997; 1998) have conducted studies on the bioavailability of selenium in pet food and pet food ingredients and found bioavailability to be low. Commercial diets contain a variety of ingredients, some of which, such as heavy metals, may interact with selenium and decrease its bioavailability (Ammerman, 1995). Commercial diets also undergo significant processing to increase shelf life.

This processing may decrease the nutritive value of the diet (National Research Council, 1986) and may have an effect on the bioavailability of selenium. Preliminary results from our laboratory have shown that when fed to cats, the bioavailability of supplemental selenium in the form of selenite or selenium yeast is twice that of selenium contained in the unsupplemented pet food.

Therefore with regard to dietary selenium intake, it seems that the present day attempt to provide cats and dogs with selenium falls short of what they would actually obtain if they were living in the wild.





Figure 3. Concentrations of total selenium in urine (μmol/L) in cats fed 0.4 or 2 ppm selenium as selenite or Sel-Plex^®.



Summary

As carnivores, cats and dogs have evolved on a diet containing selenomethionine and selenocysteine as the primary forms of selenium. Today there are a variety of commercial pet foods available for companion animals.

These diets cater more to the omnivore than the carnivore, with the inclusion of plant material in the form of cereals, grains and vegetables. Accordingly, these diets may contain forms of selenium that cats and dogs have not adapted to consume. Whether or not selenium metabolism in these species is comparable to that in omnivores has yet to be determined. Although there are no reported differences with regard to selenium deficiencies and the bioavailability of selenium in carnivores compared to omnivores, there are differences in the way cats and dogs deal with higher levels of selenium, indicating that some metabolic adjustment must have occurred in these animals. Thus while it would appear that the ideal form of selenium for the cat and dog diet is organic selenomethionine and selenocysteine, further investigation is needed as to the ideal sources and forms in which they should best be presented.



References

Ammerman, C.B. 1995. Methods for estimation of mineral bioavailability. In: Bioavailability of Nutrients for Animals, Amino Acids, Minerals, Vitamins (C.B. Ammerman, D.H. Baker and A.J. Lewis, eds). Academic Press, San Diego, CA, USA, pp. 83-94.

Anderson, H.D. and A.L. Moxon. 1942. Changes in the blood picture of the dog following subcutaneous injections of sodium selenite. J. Pharm. Exper. Therap. 76:343-354.

Beauchamp, G.K., O. Maller and J.G. Rogers, Jr. 1977. Flavor preferences in cats (Felis catus and Panthera sp.). J. Comp. Physiol. Psych. 91:1118-1127.

Boudreau, J.C. and T.D. White. 1978. Flavor chemistry of carnivore taste systems. In: Flavour Chemistry of Animal Foods. American Chemical Society (R.W. Bullard, ed). Washington, DC, pp. 102-128.

Clutton-Brock, J. 1981. Domesticated Animals from Early Times. Heinemann, London. Daniels, L.A. 1996. Selenium metabolism and bioavailability. Biol. Trace Elem. Res. 54:185-199.

Edens, F.W. and K.M. Gowdy. 2004. Selenium sources, selenoproteins and practical poultry production. In: Nutritional Biotechnology in the Feed and Food Industries, Proceedings of the 20th Annual Symposium (T.P. Lyons and K.A. Jacques, eds) Nottingham University Press, UK.

Edgar, S.E., C.A. Kirk, Q.R. Rogers and J.G. Morris. 1998. Taurine status in cats is not maintained by dietary cysteinesulfinic acid. J. Nutr. 128:751-757.

Fitzgerald, B.M. and B.J. Karl. 1979. Foods of feral house cats (Felis catus L.) in forest of the Orongorongo valley, Wellington. New Zealand J. Zoo. 6:107-126.

Forrer, R., K. Gautschi and H. Lutz. 1991. Comparative determination of selenium in the serum of various animal species and humans by means of electrothermal atomic absorption spectrometry. J. Trace Elem. Elect. Health Dis. 5:101-113.

Foster, D.J., K.L. Thoday, J.R. Arthur, F. Nicol, J.A. Beatty, C.K. Svendsen, R. Labuc, M. McConnell, M. Sharp, J.B. Thomas and G.J. Beckett. 2001. Selenium status of cats in four regions of the world and comparison with reported incidence of hyperthryoidism in cats in those regions. Amer. J. Vet. Res. 62:934-937.

Heinrich, M. and D.M. MacCanon. 1957. Some observations on the toxicity of intravenous sodium selenite in dogs. Proc. South Dakota Acad. Sci. 36:173-177.

Hendriks, W.H. and P.J. Moughan. 2000. Advances in feed evaluation for companion animals. In: Feed Evaluation Principles and Practice (P.J. Moughan, M.W.A. Verstegen and M.I. Visser-Reyneveld, eds). Wageningen Press, Wageningen, The Netherlands, pp. 269-285.

Holben, D.H. and A.M. Smith. 1999. The diverse role of selenium within selenoproteins: a review. J. Amer. Diet. Assoc. 99(7):836-841.

Jacques, K.A. 2001. Selenium metabolism in animals: the relationship between dietary selenium form and physiological response. In: Science and Technology in the Feed Industry. Proceedings of Alltech’s 17th Annual Symposium (T.P. Lyons and K.A. Jacques, eds). Nottingham University Press, UK, pp. 319-348.

Jones, E. and B.J. Coman. 1981. Ecology of the feral cat, Felis catus (L), in South-Easthern Australia 1. Diet. Austr. Wildlife Res. 8:537-547.

Kirchgessner, M., S. Gabler and W. Windisch. 1997. Homeostatic adjustments of selenium metabolism and tissue selenium to widely varying selenium supply in 75Se labeled rats. J. Anim. Physiol. Anim. Nutr. 78:20- 30.

Koller, L.D. and J.H. Exon. 1986. The two faces of selenium - deficiency and toxicity - are similar in animals and man. Can. J. Vet. Res. 50:297-306.

Levander, O.A. 1986. Selenium. In: Trace Elements in Human and Animal Nutrition (W. Mertz, ed). 5th Ed, Academic Press, Inc., London, pp. 208-279.

Lobinski, R., J.S. Edmonds, K.T. Suzuki and P.C. Uden. 2000. Species-selective determination of selenium in compounds in biological materials. Pure Appl. Chem. 72(3):447-461.

MacDonald, M.L. and Q.R. Rogers. 1984. Nutrition of the domestic cat, a mammalian carnivore. Ann. Rev. Nutr. 4:521-562.

Manktelow, B.W. 1963. Myopathy of dogs resembling white muscle disease of sheep. New Zealand Vet. J. 11:52-55.

Maskell, I.E. and J.V. Johnson. 1993. Digestion and absorption. In: The Waltham Book of Companion Animal Nutrition (I.H. Burger, ed). Pergamon Press, Oxford, England, pp. 25-44.

Mech, L.D. 1970. The Wolf: Ecology and Behaviour of an Endangered Species. The Natural History Press, New York, USA.

Morris, J.G. and Q.R. Rogers. 1989. Comparative aspects of nutrition and metabolism of dogs and cats. In: Nutrition of the Dog and Cat (I.H. Burger and J.P.W. Rivers, eds). Waltham Symposium Number 7. Cambridge University Press, Cambridge, pp. 35-66.

Morris, J.G., Q.R. Rogers and L.M. Pacioretti. 1990. Taurine: an essential nutrient for cats. In: Waltham Symposium No. 18, Health, Nutrition and Disease in Clinical Practice. 26 March, San Francisco, CA, USA.

Morris, J.G. 2002. Idiosyncratic nutrient requirements of cats appear to be diet-induced evolutionary adaptations. Nutr. Res. Rev. 15(1):153-168.

Mumma, R.O., K.A. Rashid, B.S. Shane, J.M. Scarlett- Kranz, J.H. Hotchkiss, R.H. Eckerlin, G.A. Maylin, C.Y. Lee, M. Rutzke, W.H. Gutenmann, C.A. Bache and D.J. Lisk. 1986. Toxic and protective constituents in petfoods. Amer. J. Vet. Res. 47(7):1633-1637.

National Research Council. 1985. Nutrient Requirements of Dogs. Revised edition, National Academy Press, Washington, DC.

National Research Council. 1986. Nutrient Requirements of Cats. Revised edition, National Academy Press, Washington, DC.

Oster, O., G. Schmiedel and W. Prellwitz. 1988. The organ distribution of selenium in German adults. In: Selenium: Present Status and Perspectives in Biology and Medicine (G.N. Schrauzer, ed). Humana Press Inc, USA, pp. 23-45.

Röhrs, M. 1987. Domestication of wolves and wild cats: Parallels and differences. In: Nutrition, Malnutrition and Dietetics in the Dog and Cat. Proceedings of an International Symposium (A.T.B. Edney, ed). September 3 to 4, Brit. Vet. Assoc. and Waltham Centre for Pet Nutr., Hanover, England, pp. 1-5.

Rhian, M and A.A. Moxon. 1943. Chronic selenium poisoning in dogs and its prevention by arsenic. J. Pharm. Exper. Therap. 78:249-264.

Simcock, S.E., S.M. Rutherfurd, T.J. Wester and W.H. Hendriks. 2005. Total selenium concentrations in canine and feline foods commercially available in New Zealand. New Zealand Vet. J. 53(1):1-5.

Sunde, R.A. 2000. Selenium. In: Biochemical and Physiological Aspects of Human Nutrition (M.H. Stipanuk, ed). W.B. Saunders Company, Philadelphia, PA, USA, pp. 782-809.

Surai, P. 2002. Selenium. In: Natural Antioxidants in Avian Nutrition and Reproduction. Nottingham University Press, UK, pp. 233-304.

Underwood, E.J. 1971. Selenium. In: Trace Elements in Human and Animal Nutrition (E.J. Underwood, ed). Academic Press Inc, New York, USA, pp. 323- 368.

Van Rensburg, I.B.J. and W.J.A. Venning. 1979. Nutritional myopathy in a dog. J. S. African Vet. Assoc. 50(2):119-121.

Van Vleet, J.F. 1975. Experimentally induced vitamin E-selenium deficiency in the growing dog. J. Amer. Vet. Med. Assoc. 166(8):769-774.

Wedekind, K.J., C. Cowell and G.F. Combs. 1997. Bioavailability of selenium in petfood ingredients. Fed. Proc. 11:A360.

Wedekind, K.J., R.S. Bever and G.F. Combs. 1998. Is selenium addition necessary in petfoods? Fed. Proc. 12:A823.

Wedekind, K.J., C. Kirk, S. Yu and R. Nachreiner. 2003. Defining the safe lower and upper limit for selenium in adult cats. J. Anim. Sci. 81(Suppl. 1):90.

Whanger, P.D., Y. Xia and C.D. Thomson. 1994. Protein techniques for selenium speciation in human body fluids. J. Trace Elem. Elect. Health Dis. 8:1-7.

Whanger, P.D. 1998. Metabolism of selenium in humans. J. Trace Elem. Exper. Med. 11:227-240.

Wilson, D. and S. Ruff. 1999. The Smithsonian Book of North American Mammals. Smithsonian Institution Press, Washington.

Windisch, W., S. Gabler and M. Kirchgessner. 1998. Effect of selenite, selenocysteine and selenomethionine on the selenium metabolism of 75Se labeled rats. J. Anim. Physiol. Anim. Nutr. 78:67-74.

Wolffram, S., E. Anliker and E. Scharrer. 1986. Uptake of selenate and selenite by isolated brush border membrane vesicles from pig, sheep and rat intestine. Biol. Trace Elem. Res. 10:293-306.

Wolffram, S., B. Grenacher and E. Scharrer. 1988. Transport of selenate and sulphate across the intestinal brush-border membrane of pig jejunum by two common mechanisms. Qty J. Exper. Physiol. 73:103- 111.

Wolffram, S., B. Beger, B. Grenacher and E. Scharrer. 1989. Transport of selenoamino acids and their sulfur analogues across the intestinal brush border membrane of pigs. J. Nutr. 119:706-712.

Wolffram, S. 1999. Absorption and metabolism of selenium: differences between inorganic and organic sources. In: Biotechnology in the Feed Industry, Proceedings of Alltech’s 15th Annual Symposium (T.P. Lyons and K.A. Jacquesm, eds). Nottingham University Press, UK, pp. 547-566.

Zoran, D.L. 2002. The carnivore connection to nutrition in cats. J. Amer. Vet. Med. Assoc. 221(11):1559-1567.

Readers' Rating:

Rate this article

Send to a friend