Role of Selenium in Pets Health and Nutrition: A Review
Balanced nutrition is a key element to ensure a happy and healthy life. Trace minerals are very essential nutrients in animal diet. Selenium, like the other trace minerals is necessary to sustain life of canines. Selenium is one of the critical nutritional factors for immune system along with zinc, vitamin E, vitamin B6 and linoleic acid. Adequate selenium is necessary for the normal functioning of the immune system and thyroid gland. Selenium is getting significant consideration for its role in various functions such as anticancer, joint health, skin and coat, immune resistance and antioxidant properties etc. Selenium forms the active center for selenoenzymes that carryout redox reactions such as glutathione peroxidase (GPx), thioredoxin reductase, thyroid hormone deiodinase and so on. Animal studies have shown a beneficial effect of selenium in the prevention of cancer. Selenium deficiency has become increasingly recognized as a practical problem in animal industry. Insufficient selenium intake can cause serious health problems, including Kashin-Beck disease in human beings, which is characterized by the degeneration of the articular cartilage between joints, thyroid disease and a variety of cancers. Selenium supplementation is required to overcome the deficiency symptoms and the bioavailability of the same depends upon the nature of supplements used. It is generally found that organoselenium compounds have substantially greater bioavailability than that of inorganic selenium.
Received: April 22, 2010;
Accepted: May 25, 2010;
Published: July 27, 2010
Selenium, like the other trace minerals is necessary to sustain life and is
essential for basic physiological functions in both animals and humans. While
the daily requirement for this mineral is obviously less, its importance and
impact on the health and well being of livestock and humans are well documented
in research. It was discovered in 1817 by Swedish chemist (Mugesh
and Singh, 2000). It was considered as a poison until identified as a micronutrient
for bacteria, mammals and birds (Schwarz and Foltz, 1957).
It has been found to be present in at least 15 different mammalian selenoproteins
and up to seven microbial selenoenzymes so far (Sunde, 1997).
The animal body is under constant attack from free radicals, formed as a natural
consequence of the bodys normal metabolic activity and as part of the
immune systems strategy for destroying invading microorganisms. It has
been calculated that about 2x1010 molecules of Reactive Oxygen Species
(ROS) are generated per cell per day (Chance et al.,
1979). These reactive species are involved in the initiation, propagation
and maintenance of both acute and chronic inflammatory processes (Halliwell
et al., 1982; Mugesh and Singh, 2000). Ultimately
this leads to aging, Alzheimer disease, inflammation and certain types of cancer.
There is a need for defensive action against these reactive species. An antioxidant
may be defined as any substance that when present at low concentrations, compared
with those of the oxidizable substrate, significantly delays or inhibits oxidation
of that substrate (Gutteridge, 1994). Antioxidants
play an important role since they protect the cells from oxidative cell damage.
Scientific evidence suggests that antioxidants reduce the risk for chronic diseases
including cancer and heart disease. The main characteristic of an antioxidant
is its ability to trap free radicals. Antioxidants which scavenge the active
oxygen species are found in variety of food stuff. Selenium has been known to
be intimately involved in the activity of enzymes such as glutathione peroxidase
(Gpx) and thioredoxin reductase and protect the biomolecules against reactive
oxygen species and free radical damage (Nordberg and Arner,
Dietary sources are the good sources of selenium for the body and supplements
are needed for the consumers living in the areas that are deficient of selenium.
Selenium deficiencies have been reported to suppress the immune response in
various species (Sheffy and Schultz, 1979). Selenium
deficiency reduces T-cell dependent antibody responses, which further gets magnified
with vitamin E deficiency. Several metabolic disorders have been reported due
to the dietary deficiencies of selenium and vitamin E in several species like
chickens (Schwarz et al., 1957), turkeys (Scott
et al., 1967), rats (Schwarz and Foltz, 1957),
calves, lambs with several health disorders. Current selenium supplements rely
on inorganic forms such as sodium selenite (Na2SeO3) or
sodium selenate (Na2SeO4). Organoselenium compounds have
been found to be an alternative to inorganic selenium compounds with greater
bioavailability (Jacob et al., 2004). More importantly,
organic selenium is usually found to be less toxic than inorganic forms (Narajji
et al., 2007; Arenholt-Bendsleve et al.,
1988). The margin between its protective role and adverse effect is very
low and depends on the form of selenium being used.
Role of selenium in dogs: Research studies to date have indicated that
selenium does have beneficial physiological effects on mammals. For example,
it is known that selenium, when ingested, reduces the rate of oxidative damage
caused by chemicals, by entering the membranes of the body's cells and protecting
the contents of the cells from reacting with oxygen in a manner that damages
the cells. Selenium deficiency may be associated with a myopathy in dogs (Manketlow,
1963). The diet of these dogs was principally mutton from an area of New
Zealand where selenium-responsive diseases of sheep were noted. A fatal, myocardial
necrosis was seen in young pups and a skeletal myodegeneration in an adult dog.
Two bitches that had lost litters during previous perinatal periods were dosed
with selenium during pregnancy and subsequently whelped normal litters.
Synergistic effect of selenium with vitamin E was observed when administered
together to Beagles. It was demonstrated that Beagles which were initially 5
to 8 weeks old, developed clinical signs of vitamin E-selenium deficiency after
40 to 60 days of consuming an unsupplemented semisynthetic diet (Van
Vleet, 1975). Generalized muscular weakness progressed from unsteadiness
to prostration and coma. In a case study it was observed that multiple severe
deaths due to acute myocardial degeneration occurred in a commercial kennel.
Further losses were prevented when vitamin E and selenium supplementation was
instituted (Green and Lemckert, 1977).
Selenium has been found to reduce incidences of cancer in both dogs and human.
Selenium supplementation has shown to decrease DNA damage and increase epithelial
cell apoptosis within the aging canine prostate (Waters
et al., 2003). Research suggests that selenium also helps with improving
long-term joint health and can reduce risks of Kashin-Beck disease (Sudre
and Mathieu, 2001; Levander and Beck, 1997; Beck
et al., 2003) which involves the articular cartilage between joints
degenerating, thyroid disease and cancers. Selenium is also thought to help
prevent hip dysplasia (Hamilton, 1999).
Selenium can increase the health of the skin, potentially reducing dandruff
and dry skin. It plays an important role in hair growth. Selenium can also improve
the hair coat quality, making it more soft and shiny. As a result of a healthier
coat, there is also the possibility of less shedding and hair loss. In a study
conducted by Yu et al. (2006) it was demonstrated
that both low and high selenium in diet reduced hair growth in adult dogs.
Pet animals obtain dietary selenium from cereals and grains, or from the tissues
of other animals, depending on dietary habit. The forms of dietary selenium
from both plant and animal sources include a range of inorganic and organic
selenium compounds (Whanger, 2002). 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).
Biochemical role of selenium in mammals is clearly established. It forms the
active center for selenoenzymes. Glutathione peroxidase is one such enzyme which
contains selenol (-SeH) group in the active center. Glutathione peroxidase catalyzes
the oxidation of reduced glutathione and allows for the reduction of hydrogen
peroxide to water, preventing lipid peroxidation and cellular damage (Rotruck
et al., 1973). The GPx catalytic site includes a Selenocysteine residue
in which the selenium undergoes a redox cycle involving the selenol (ESeH) as
the active form that reduces hydrogen peroxides and organic peroxides. Selenocysteine
is known as 21st amino acid (Rayman, 2005). It is located
in the N-terminal end of helix α1 (Epp et
al., 1983). The selenol is oxidized to selenenic acid (ESeOH), which
reacts with reduced glutathione (GSH) to form a selenenyl sulphide adduct (ESeSG).
A second glutathione then regenerates the active form of the enzyme by attacking
the ESeSG to form the oxidized glutathione (GSSG). Thus, in the overall process,
two equivalents of glutathione are oxidized to the disulphide and water, while
the hydroperoxide is reduced to the corresponding alcohol as shown in Fig.
1 (Roy et al., 2005).
|| Schematic diagram of proposed catalytic mechanism for reduction
of hydroperoxides by Gpx
|| Selenium levels in different food items
|*DV: Daily value. DVs are reference numbers developed by the
Food and Drug Administration (FDA) to help consumers determine if a food
contains a lot or a little of a specific nutrient. The DV for selenium is
70 μg. Most food labels do not list a food's selenium content. The
percent DV (%DV) listed on the table indicates the percentage of the DV
provided in one serving. A food providing 5% of the DV or less is a low
source while a food that provides 10-19% of the DV is a good source. A food
that provides 20% or more of the DV is high in that nutrient. It is important
to remember that foods that provide lower percentages of the DV also contribute
to a healthful diet. For foods not listed in this table, please refer to
the U.S. Department of Agriculture's Nutrient Database Web site: http://www.nal.usda.gov/fnic/cgi-bin/nut_search.pl
Finally glutathione disulfide gets reduced by NADPH which is catalyzed by glutathione reductase. This results in the formation of glutathione.
Nutritional forms of selenium: The Brazil nut (Bertholletia excelsa)
which is a South American tree in the family Lecythidaceae have relatively high
selenium concentrations (Table 1). Foods of low protein content,
including most fruits and vegetables, provide little selenium (Simcock
et al., 2005).
Selenium and pet food diets: Fish, meat, poultry, whole grains and dairy
products are typical sources of this nutrient. AAFCO and the FDA have approved
a selenium supplement to animal diets, most commonly in the form of sodium selenite
for pet foods. It has been observed that inorganic selenium is less available
when the animal is under stress. In addition, there is a significant loss of
selenium after periods of stress, making selenium levels in the blood less stable.
Depending on the nature of ingredients used in pet food formulations, the selenium
levels vary in all diets. Research (Fan and Kizer, 1990;
Olson, 1986) proved that inorganic selenium sources can be toxic in high
doses; affecting an animals blood, liver and muscles. Inorganic selenium
cannot be fully metabolized or stored in the body. Consequently, selenium deficiencies
still arise in animals that are supplemented with inorganic selenium (Lopez
et al., 1969).
SELENIUM METABOLISM IN MONOGASTRIC SPECIES
The wild dog would 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 depends on the part of the animal consumed and its metabolic pathway as indicated in Fig. 2. 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.
Since, cat generally consumes a diet of whole prey such as rats or mice, the forms of selenium ingested would be in the form of 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 AAFCO has defined he minimum selenium requirement in cats and dogs (Table 2).
Hence, animal tissues play a primary role as source of dietary selenium for both cats and dogs, i.e., the organic forms of selenomethionine and selenocysteine. The pets which are fed with commercial diets 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 in pet foods is highly variable.
Most dry and canned dog foods today use an inorganic type of selenium, sodium
selenite or sodium selenate. In addition to selenium present in the pet food
ingredients, additional selenium sources are added in commercial diet formulations.
Selenite (Forceville and Meaux, 2007) was found to have
a pro-oxidant effect and therefore the use of selenate was preferred.
|| Overview of selenium metabolism in monogastric species
|| Selenium nutrient profiles as published in 2008a
by AAFCO for dog and cat food
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 in the body.
The role of trace mineral selenium in animals particularly pets is discussed and reviewed. Selenium deficiency is found to be one of the key factor behind many diseases like Kashin beck disease, cardiomyopathy, etc., Selenium levels and its forms in the diets play an important role in managing the trace mineral level in the body of the pet animal. However, toxicity associated with the high dose of selenium makes it vulnerable to pets and other animals due to the narrow difference between its required dose and the toxic dose. Current selenium supplements are mainly dependent on inorganic sources like sodium selenite which are found to be less bioavailable and also toxic. However, relative uses of selenium and its forms would be dependent on its nature of application and end use requirement. Keeping safety of the pet animals and environment as main focus areas, organoselenium compounds would be a good and alternate prospective choices for research scientists working in pet animal nutrition.
1: Arenholt-Bendsleve, D., M. Abdulla, A. Jepsrn and E. Pedeson, 1988. Effect of organic and inorganic selenium on human keratinocytes. Trace. Elem. Med., 5: 29-34.
2: Beck, M.A., O. Levander and J. Handy, 2003. Selenium deficiency and viral infection. J. Nutr., 133: 1463-1467.
PubMed | Direct Link |
3: Chance, B., H. Sies and A. Boveris, 1979. Hydroperoxide metabolism in mammalian organs. Physiol. Rev., 59: 527-605.
PubMed | Direct Link |
4: Epp, D., R. Landenstein and A. Wendel, 1983. The refined structure of the selenoenzyme glutathione peroxidase at 0.2 nm resolution. Eur. J. Biochem., 133: 51-69.
5: Fan, A.M. and K.W. Kizer, 1990. Selenium. nutritional, toxicologic and clinical aspects. West J. Med., 153: 160-167.
6: Forceville, X. and C.H. Meaux, 2007. Effects of high doses of selenium, as sodium selenite, in septic shock patients a placebo-controlled, randomized, double-blind, multi-center phase II study-selenium and sepsis. J. Trace Elem. Med. Biol., 21: 62-65.
7: Green, P.D. and J.W.H. Lemckert, 1977. Vitamin E and selenium responsive myocardial degeneration in dogs. Can. Vet. J., 18: 290-291.
8: Gutteridge, J.M.C., 1994. Free radicals and aging. Rev. Clin. Gerontol., 4: 279-288.
9: Halliwell, B., J.R. Hoult and D.R. Blake, 1982. Oxidants, inflammation and anti-inflammatory drugs. FASEB J., 2: 2867-2873.
10: Jacob, J.H., A.M. Khalil and A.O. Maslat, 2004. In vitro cytogenetic testing of an organoselenium compound and its sulfur analogue in cultured rat bone marrow cells. J. Carcinog., 3: 5-13.
CrossRef | PubMed | Direct Link |
11: Levander, O.A. and M.A. Beck, 1997. Interacting nutritional and infectious etiologies of Keshan disease: Insights from coxsackie virus B-induced myocarditis in mice deficient in selenium or vitamin E. Biol. Trace Elem. Res., 56: 5-21.
12: Lobinski, R., J.S. Edmonds, K.T. Suzuki and P.C. Uden, 2000. Species-selective determination of selenium compounds in biological materials. Pure Applied Chem., 72: 447-461.
Direct Link |
13: Manketlow, B.W., 1963. Myopathy of dogs resembling white muscle disease of sheep. N. Z. Vet. J., 11: 52-55.
14: Mugesh, G. and H.B. Singh, 2000. Synthetic organoselenium compounds as antioxidants: Glutathione peroxidase activity. Chem. Soc. Rev., 29: 347-357.
15: Narajji, C., M.D. Karvekar and A.K. Das, 2007. Biological importance of organoselenium compounds. Indian J. Pharm. Sci., 69: 344-351.
Direct Link |
16: Nordberg, J. and E.S.J. Arner, 2001. Reactive oxygen species, antioxidants and the mammalian thioredoxin system. Free Radic. Biol. Med., 31: 1287-1312.
CrossRef | PubMed | Direct Link |
17: Olson, O.E., 1986. Selenium toxicity in animals with emphasis on man. Int. J. Toxicol., 5: 45-70.
18: Lopez, P.L., R.L. Preston and W.H. Pfander, 1969. Whole-body retention, tissue distribution and excretion of Selenium-75 after oral and intravenous administration in lambs fed varying selenium intakes. J. Nutr., 97: 123-132.
Direct Link |
19: Rayman, M.P., 2005. Selenium in cancer prevention: A review of the evidence and mechanism of action. Proc. Nutr. Soc., 64: 527-542.
20: Rotruck, J.T., A.L. Pope, H.E. Ganther, A.B. Swanson, D.G. Hafeman and W.G. Hoekstra, 1973. Selenium: Biochemical role as a component of glutathione peroxidase. Science, 179: 588-590.
CrossRef | PubMed | Direct Link |
21: Roy, G., B.K. Sarma, P.P. Phadnis and G. Mugesh, 2005. Selenium-containing enzymes in mammals: Chemical perspectives. J. Chem. Sci., 117: 287-303.
22: Schwarz, K., J.G. Bieri, G.M. Briggs and M.L. Scott, 1957. Preventions of exudative diathesis in chicks by Factor 3 and selenium. Proc. Soc. Exp. Biol. Med., 95: 621-625.
23: Schwarz, K. and C.M. Foltz, 1957. Selenium as an integral part of factor 3 against dietary liver degeneration. J. Am. Chem. Soc., 79: 3292-3293.
Direct Link |
24: Scott, M.L., G. Olson, L. Krook and W.R. Brown, 1967. Selenium-responsive myopathies of myocardium and smooth muscle in the young poultry. J. Nutr., 91: 573-583.
Direct Link |
25: Sheffy, B.E. and R.D. Schultz, 1979. Influence of vitamin E and selenium on immune response mechanisms. Fed. Proc., 38: 2139-2143.
26: 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. N. Z. Vet. J., 53: 1-5.
27: Sudre, P. and F. Mathieu, 2001. Kashin-beck disease: From etiology to prevention or from prevention to etiology. Int. Orthop., 25: 175-179.
28: Sunde, R.A., 1997. Selenium. In: Handbook of Nutritionally Essential Mineral Elements, O'Dell, B.L. and R.A. Sunde (Eds.). Marcel Dekker, New York, pp: 493-556
29: Van Vleet, J.F., 1975. Experimentally induced vitamin E-selenium deficiency in the growing dog. J. Am. Vet. Med. Assoc., 166: 769-774.
30: Waters, D.J., S. Shen, D.M. Cooley, D.G. Bostwick and J. Qian et al., 2003. Effects of dietary selenium supplementation on DNA damage and apoptosis in canine prostate. J. Nat. Cancer Inst., 95: 237-241.
31: Whanger, P.D., 2002. Selenocompounds in plants and animals and their biological significance. J. Am. College Nutr., 21: 223-232.
Direct Link |
32: Yu, S., K.J. Wedekind, C.A. Kirk and R.F. Nachreiner, 2006. Primary hair growth in dogs depends on dietary selenium concentrations. J. Anim. Physiol. Anim. Nutr., 90: 146-151.
33: Hamilton, D., 1999. Homeopathic Care for Cats and Dogs: Small Doses for Small Animals. North Atlantic Books, California, USA., ISBN-13: 978-1556432958