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The role of selenium in companion animal health and nutrition |
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Author: S.E. SIMCOCK, S.M. RUTHERFURD AND W.H. HENDRIKS - Massey University (Courtesy of Alltech Inc.)
Publication date: 12/19/2006
Introduction
Companion animals are members of the order Carnivora, meaning ‘flesh-eaters’, although this order also includes herbivores, omnivores and strict carnivores. The omnivorous diet of the dog throughout evolution is believed to have contained animal and plant material while in contrast, the cat is believed to have evolved as an obligate carnivore.
For this reason, the cat has several unique adaptations to protein, fatty acid and vitamin metabolism (MacDonald et al., 1984; Hendriks, 1998; Lowe and Markwell, 1995) and is therefore less likely to adapt to a varied dietary composition than the omnivorous dog.
There is a lack of data on the metabolism of minerals in companion animals. Hendriks (1998) constructed tables from the literature showing the minimum mineral requirements of growing kittens and adult cats. A comparison was made of the minimum mineral requirements for dogs, rats and cats, which showed that the quantitative requirements for essential minerals were similar in magnitude in these three species. This suggests that mineral metabolism in cats may be similar to that of other species. There are a number of minerals (e.g. selenium) for which the essentiality remains to be proven in both dogs and cats, but it is generally assumed that cats and dogs require these minerals in amounts similar to other species. However, given the unique characteristics of other aspects of feline metabolism, it is possible that there will be differences in the transport and storage of minerals in felines (MacDonald et al., 1984).
The present contribution will focus on reviewing the nutrition and metabolism of selenium (Se) in cats and dogs. In addition, data are presented on total Se levels in commercially available feline and canine diets.
Selenium metabolism
FORMS OF SELENIUM
Selenite and selenate are inorganic Se salts, which are often used to supplement diets. Plants absorb inorganic Se from the soil and convert it to organic selenoamino acids such as selenomethionine (the main form) and selenocysteine, which can be incorporated into protein. Consequently, organic Se is a component of many grains and forages and is often found in feed ingredients. Selenium derived from selenoamino acids or selenoproteins present in the diet can also be found in animal tissue where it is either stored or involved in antioxidant functions, thyroid metabolism, sperm structure and perhaps many other functions that have yet to be identified.
ABSORPTION
Absorption of Se occurs in the small intestine, mainly the duodenum, with the mechanism depending on the form of Se. Selenate is actively absorbed by co-transport with sodium ions and it shares this carrier-mediated mechanism of absorption with sulfate (Wolffram et al., 1986; Wolffram et al., 1988). Selenite does not have to compete with sulfate and is absorbed by passive diffusion (Wolffram et al., 1986). Organic amino acid-bound Se (selenomethionine and selenocysteine) is actively absorbed across the intestine via a specific sodiumdependent amino acid transport system (Wolffram et al., 1989a; 1989b). Absorption of these selenoamino acids is competitively inhibited by methionine and cysteine, respectively, as they share the same transport mechanisms. These different absorption mechanisms are reflected in the rate of absorption of each form of Se. This was illustrated by Reasbeck et al. (1985) in a gut perfusion experiment in adult dogs. These authors found that absorption of selenomethionine was significantly greater than that of selenocysteine, whilst selenite absorption was the slowest of the three forms.
Approximately 90% of Se was absorbed when administered as selenite in adult dogs (Furchner et al., 1975). However no published data are available on mechanisms or rates of Se absorption in cats.
METABOLIC FATE AND TISSUE DISTRIBUTION OF ABSORBED SE
Once absorbed, dietary Se of inorganic or organic origin has different metabolic fates, resulting in storage, selenoprotein synthesis or excretion (Jacques, 2001). All dietary forms of Se are converted to a common form of Se, hydrogen selenide, before they can be used in selenoprotein synthesis (Levander and Burk, 1996) (Figure 1).
Selenomethionine not immediately used is incorporated into body proteins for storage, or is taken up by organs and tissues with high rates of protein synthesis (Schrauzer, 2000).
There have been several studies in dogs and cats that illustrate tissue distribution of Se. Using radiolabelled Se (75Se-methionine), Meinhold et al. (1975) found significant amounts of 75Se-met in the pancreas, liver and kidney of an adult and a growing dog. Boyer et al., (1978) fed kittens a diet of commercially canned red tuna, which is thought to contain high levels of Se (Furr et al., 1976; NRC, 1986), for 100 days. The levels of Se in various tissues of the tuna-fed kittens were compared with those of kittens fed a control diet. On average, Se levels in the brain increased 1.5-fold and in muscle 3-fold, while in blood, bone, kidney and spleen Se increased at least 6-fold (Table 1). The greatest increase in Se content, of almost 9-fold, was seen in the liver.
Blood
Se levels of control kittens in the Boyer et al. (1978) study are the same as those given in a summary of diagnostic data by Puls (1988) for adequate levels of whole blood Se in cats. Similarly, levels stated as high by Puls (1988) are the same as those seen in the tuna-fed kittens in Boyer et al.
(1978), indicating that the data from Puls (1988) may have been obtained from this study. Puls (1988) also gave ranges for adequate and high levels of Se in the liver and kidney of cats (ppm, wet weight): liver – adequate: 0.26 – 0.54, high: 2.00 – 4.60; kidney – adequate: 0.77 –1.14, high: 4.20 – 9.40.
Figure 1. Dietary selenium metabolism in animals (Jacques, 2001).
Table 1. Selenium levels in tissues of kittens after 100 days on a diet of canned red meat, tuna or dry cat food.
Adapted from Boyer et al. (1978).
How these estimates were derived was not stated. Smith et al. (1937) studied chronic selenium poisoning in adult cats given 0.1 or 0.25 mg Se/kg from sodium selenite. These authors found a wide distribution of selenium throughout the body tissues, with highest concentrations in the liver, kidney, spleen, pancreas, heart and lungs. Erythrocytes were found to contain more selenium than plasma. In another study, increased levels of Se were found in the lung, kidney, liver, blood, spleen and heart tissue of adult Beagle dogs following inhalation of selenious acid (Weissman et al., 1983). Since large amounts of Se were found in the liver, its significance as a major site for metabolism was suggested. Hepatic liver Se concentrations in dogs ranged from approximately 1.25 – 3.25 μg/g and these levels were found to decrease with age (Keen et al., 1981).
Selenium not required for selenoprotein formation or stored in tissues is methylated and excreted (Figure 1). Excretion occurs mainly via the urine but also in the faeces and via the lungs (Underwood and Suttle, 1999; Jacques, 2001). In contrast to selenomethionine, dietary inorganic Se is not taken up by tissues or stored (Schrauzer, 2000), so any amount surplus to selenoprotein synthesis requirements is also excreted (Jacques, 2001).
Smith et al. (1937) administered 0.1 – 0.25 mg Se/kg from sodium selenite to adult cats orally or subcutaneously for up to 188 days. Fifty to 80% of the total Se was usually excreted in the urine, and from traces to 18% was excreted in faeces. More Se was excreted in the faeces when it was given orally than when given subcutaneously. A relationship was found between Se concentration in the urine and the daily dose administered in chronic Se poisoning (Smith et al., 1937). To determine retention of Se in the body following chronic Se poisoning, adult cats were given 0.1 mg Se/kg from sodium selenite over a period from 168 to 175 days. Most of the stored Se was eliminated within 2 weeks after administration ceased. Small amounts of Se were found in the urine and some other tissues, especially the liver, for at least a month (Smith et al., 1937).
Selenium in health and disease
TOXICITY
Signs of toxicity in dogs include refusal of food leading to weight loss, anorexia and stunted growth, nausea and vomiting, diarrhoea, apprehension, respiratory stimulation and cardiovascular changes (Anderson et al., 1942; Rhian et al., 1943; Heinrich and MacCanon 1957). In more severe cases, nervous disorders and pathological lesions may develop with the liver and spleen being the most affected organs (Rhian and Moxon, 1943). In extreme cases death may occur (Anderson and Moxon, 1942).
Rhian and Moxon, (1943) found that signs of toxicity occurred when 7.2 or 10 ppm Se added as sodium selenite were included in the diet of growing and adult dogs. Sodium selenite given at 20 ppm Se caused death in a very short time. The minimum lethal dose of sodium selenite administered by intramuscular injection for dogs is 2 mg/kg body weight (NRC, 1976).
Studies in anaesthetized and unanaesthetized adult dogs found that a combination of pentobarbitone and oxygen, as well as oxygen alone, increased the toxicity of selenite (Anderson and Moxon, 1942; Heinrich and MacCanon, 1957). Doses of selenite between 0.1 and 1 mg/kg were usually fatal to anaesthetized dogs breathing oxygen within 7 hrs of administration, whereas the same doses were not fatal to dogs breathing room air (Heinrich and MacCanon, 1957). The minimum lethal dose for dogs under barbital depression was found to be between 1.5 and 2 mg/kg (Anderson and Moxon, 1942). Consequently, oxygen appears to cause increased sensitivity to Se toxicity in anaesthetized dogs (Heinrich and MacCanon, 1957). Conversely, pentobarbital anaesthesia may offer some protection. Heinrich and MacCanon (1957) suggested that central nervous stimulation is responsible for the symptoms of Se toxicity, and that this central stimulation may be antagonized by pentobarbitone.
Selenium interacts with other substances in the diet such as vitamin E, sulfur amino acids and heavy metals, and in some cases the effects of Se toxicity are counteracted. When growing dogs were fed 13 ppm Se, 5 ppm arsenic added to drinking water counteracted or prevented the symptoms of chronic Se poisoning (Rhian and Moxon, 1943).
In diagnostic data published by Puls (1988), the minimum lethal dose of Se for cats was reported to be 1.5 – 3.0 mg/kg body weight, regardless of route of administration. No references are provided as to where these estimates were obtained.
DEFICIENCY
There have been some reports of Se deficiency in dogs but there have been no accounts in cats.
Clinical signs of Se deficiency in growing dogs include muscular weakness, subcutaneous oedmea, anorexia, depression, dyspnea and eventual coma (Van Vleet, 1975). This author also found pathological signs, which included extensive muscular degeneration, necrosis in the myocardium and renal mineralisation. Manktelow (1963) and Van Rensburg (1979) reported similar lesions in growing and adult dogs with Se deficiency. The lesions resembled those seen in lambs with white muscle disease (Van Rensburg and Venning, 1979).
HEALTH
Selenium has an extensive role in antioxidant defence and is also an important factor in thyroid function, growth and fertility. Much research has been conducted on the anti-tumorigenic activities of Se. The use of established cell lines in dogs provides a good model to study Se-induced inhibition of tumor growth (Fico et al., 1986).
Hyperthyroidism is a common endocrine disease in cats and it is thought that Se plays an important role in homeostasis of the thyroid gland. Foster et al. (2001) conducted a study to assess the Se status of cats in four locations (Edinburgh, Sydney, Denmark and Perth) and compared this with reports of hyperthyroidism in cats from those regions.
Plasma Se concentrations were found to range from 3.95 to 8.70 mmol/l in cats from the four areas. There was no significant difference in plasma Se level of the cats among the four different regions and the authors concluded that Se status alone did not affect the incidence of hyperthyroidism in cats.
Conversely, hypothyroidism is a common disease of dogs. Low Se intake impairs the activity of iodothyronine 5′deiodinase, which catalyses the deiodination of thyroid hormones. Wedekind et al. (2001) studied the effect of varying Se intake on thyroid hormone metabolism in adult dogs. Dogs were depleted of Se then supplemented with different levels of selenomethionine. These authors measured Se concentrations and glutathione peroxidase (GSH-Px) activities in serum and red blood cells as well as thyroid profiles and antithyroid activities. Thyroid levels were normal, but T3 increased with increase in Se intake. Autoimmune measures showed no effect of Se intake. Their results suggested that Se deficiency was not a major factor in the etiology of canine hypothyroidism.
Selenium bioavailability
DEFINITION
The bioavailability of a nutrient can be defined as “the proportion of a dietary nutrient being absorbed across the gastrointestinal epithelium which can be utilised by the animal” (Hendriks, 1998). This definition is generally used for amino acids. For minerals, availability is the most useful measure.
Measurements of the bioavailability of Se-containing amino acids and the availability of inorganic Se sources are a means of quantifying the usefulness of dietary Se to the animal. This information is important when formulating a diet as it facilitates the fulfillment of specific nutritional requirements.
BIOAVAILABILITY STUDIES
Wedekind and Combs (1999a) conducted several studies to determine Se availability in chickens, kittens and puppies. Chick bioassays were used to determine the availability of Se in various pet food ingredients and diets. Chicks were fed a low Se diet to deplete Se stores and then supplemented with various known amounts of sodium selenite to create a standard curve. Sodium selenite was given a value of 100% to enable quantification of the relative availability of Se in test ingredients. Selenium and GSH-Px concentrations were measured in serum and liver. Results showed the following availabilities of Se: beef lung 19%, beef spleen 38%, beef tongue 15%, mackerel 9%, eggs 33%, poultry by-product meal 15%, pork liver 25%, feline canned food 17%, canine canned food 25% and canine dry diets 21% (Wedekind et al., 1997). Relatively low availabilities of Se were seen for animal-derived ingredients (28%), higher availabilities for plant-derived ingredients (47%) and very high (159%) availabilities for Se-enriched yeast. Availabilities of Se in canned diets (30%) were lower than for extruded diets (53%) (Wedekind et al., 1998). These studies indicate that the (bio)availability of Se is often low in pet foods; and the latter authors suggest that Se supplementation may be required in many cases.
Availability studies in kittens and puppies (Wedekind et al., 1999; 2000) suggested that the minimum requirements estimated by AAFCO and NRC were too low, as is discussed in the following section.
Selenium requirements
Selenium has been proven to be a dietary essential mineral in many species including dogs, but not cats. In 1986 when the National Research Council (NRC) was updating its minimum requirements for cats, no data had been published with regard to Se. Thus minimum Se requirements were estimated by extrapolation of the requirements in other species (NRC, 1986). Relatively more data were available on the Se requirements for dogs (NRC, 1985) based mainly on deficiency studies in Beagle puppies by Van Vleet (1975).
A minimum Se requirement for cats was estimated to be 100 μg Se/kg diet by the NRC (1986).
However this estimate does not take into account the availability of Se in pet foods or pet food ingredients. The availability studies conducted by Wedekind et al. (2000) indicated that the minimum dietary Se requirement should be higher, and it was suggested commercial diets for growing kittens contain a minimum level of 0.4 mg/kg diet. It is possible that requirements differ with physiological stage such as the maintenance, reproduction and geriatric stages (Shields, 1998).
NRC recommendations for dogs include a minimum nutrient requirement of 6 μg Se/kg body weight for growth and 2.2 μg/kg for adult maintenance (NRC, 1985). Based on the work by Van Vleet (1975), a dietary concentration of 0.3 mg Se/1000 kcal metabolisable energy (ME) meets the requirements for growing dogs consuming a diet with adequate vitamin E levels, or up to 0.5 mg/kg if vitamin E levels are limited (NRC, 1985). Once again, availability of Se was not considered in these estimates. Wedekind et al. (1999b) conducted availability studies in Beagle puppies and recommended a minimum level of 0.2 mg/kg diet for growing dogs.
In the past, Se requirements have been portrayed as minimum levels. However with the knowledge of the toxic effects of this element, the use of optimum ranges have become increasingly important (Shields, 1998). This was recognized by AAFCO in 1993 when they changed from using minimum requirements to more optimum levels.
AAFCO now also provide recommendations for two life stages: growth and reproduction, and maintenance (AAFCO, 2000).
Table 2. AAFCO Se profiles for dogs and cats.
As more information becomes available about the functions of Se, and as more precise methods of assessing Se status are identified, requirement estimates will need to be continually updated (Shields, 1998).
Selenium in the diet
Commercial pet foods can be divided into three categories based on the water content of the food: dry (<10% moisture), semi-moist (10-40% moisture) and moist (40-80% moisture). Dog and cat foods often contain a wide variety of ingredients including animal, poultry, cereal, plant by-products, meat, meat by-products and added nutrients (Mumma et al., 1986). Knowledge of the nutrient requirements of the animal, the composition of the ingredients and the bioavailability of the nutrients in the ingredients are needed to formulate a well-balanced pet food (Dzanis, 1994).
If Se is added to pet foods, it is usually added in the form of the inorganic sodium selenate or sodium selenite. The Se content of sodium selenite and sodium selenate are 45.6% and 41.8% respectively (NRC, 1986).
Mumma et al. (1986) measured the mineral levels in several dog and cat foods. Selenium content ranged from 0.07 - 0.65 mg/kg dry matter in dog food and 0.27 - 6.10 mg/kg dry matter in cat food.
Furthermore, the Se content of certain constituents of pet foods was reported by Furr et al. (1976) on a fresh weight basis (mg/kg diet): cereals and grains, 0.02-1.1; marine fish, 0.1-2.0; meats, 0.2-4.2 and vegetables, 0-0.6 mg/kg.
Plasma Se concentrations in adult cats have been reported to be up to 5-fold higher than in other animals (Koller and Exon, 1986; Forrer et al., 1991).
High concentrations of Se have been found in pet foods containing tuna (Furr et al., 1976).
Consequently, if cats are fed tuna-based diets this may explain their unusually high Se levels. However there have been no reports of Se toxicity in growing or adult cats (Boyer et al., 1978). This tolerance of cats to Se may be explained by the high amounts of mercury found in tuna based cat foods (Boyer et al., 1978), by a low (bio)availability of the Se in the food or it may be associated with some unique aspect of Se metabolism in this species.
SUMMARY
The current literature lacks data on Se metabolism and its relationship with nutrition and health in companion animals. Some information has been published on absorption of Se in dogs; and there are also data available on the tissue distribution of Se in adult and growing dogs and cats. However there is no information on metabolism of Se in cats, and data on other aspects of metabolism in dogs are lacking. Limited data are available on normal Se levels in cats and dogs and more comprehensive reference values would be useful. Several toxicity and deficiency studies have been performed in dogs, but little data have been published in cats. Availability studies in growing cats have been documented but more information is needed on the availability of Se in adult animals. Furthermore, there is a need for more information on Se requirements for both cats and dogs in the growing and maintenance stages.
Total Se content in a range of commercial pet foods: preliminary data
This study aimed to survey the Se content of a wide range of commercial pet foods. This information can then be used to investigate normal dietary levels consumed by cats and dogs.
MATERIALS AND METHODS
Sample preparation and analysis
A range of approximately 90 pet food samples was obtained from local supermarkets and vet clinics in Palmerston North, New Zealand. The samples were complete pet food diets produced in New Zealand, Australia and the US. Dried foods were finely ground using a kitchen coffee grinder. Each ground sample was mixed thoroughly and stored in plastic bags at –20 °C prior to Se analysis. Moist foods were freeze-dried and then ground and stored as described for dry foods.
Samples were analysed using a fluorometric method based on the AOAC official method (2000) and the methods of Sheehan and Gao (1990). The samples were digested in 0.5 ml of a nitric acidperchloric acid mixture (4:1 by volume) and reduced to selenite with 0.5 ml HCl. The piazselenol was formed after addition of 0.5 ml of 2,3- diaminonaphthalene, and was extracted with 3 ml of cyclohexane for 10 minutes. The Se content was determined from the extract using a scanning fluorescence detector (λex 375 nm, λem 525 nm).
Data were quantified using Millenium32 version 3.05.01.
Each sample was analysed in quadruplicate due to the heterogeneous nature of the sample. For samples where the coefficient of variation exceeded 10%, the analysis was repeated. With each set of samples a reagent blank, 6 selenite calibrating standard solutions (0 – 0.1 ml) and a commercially available certified reference material (CRM) was used. The CRM was freeze-dried bovine blood (A-13) from Analytical Quality Control common ingredient in cat foods, followed by chicken, meat mix, chicken and seafood, ‘other’ and finally beef.
Figure 2. Total selenium content (mg/kg) of petfoods categorised according to petfood type.
For all ingredient types, cat foods contained higher concentrations of Se than dog foods (Figure 3).
Seafood-based foods contained the highest mean Se concentrations and widest range of Se values.
Foods containing a combination of chicken and seafood had the next highest levels and the remaining ingredient types showed similar concentrations in dog foods or cat foods.
The predominant finding from this study was the high levels of Se and the high degree of Se variability found in cat foods, particularly wet cat foods, compared with dog foods. Seafood was the most common ingredient of the cat food samples analysed, and seafood samples contained the highest levels of Se. Other authors have also shown high levels of Se in seafood or seafood diets (Furr et al., 1976; NRC, 1986; Forrer et al., 1991; Mumma et al., 1986). Thus it is likely that the high Se concentrations and greater range of Se concentrations found in the seafood-based cat foods analysed in this study were due to a high, and perhaps variable, seafood content in the diet. In contrast, dog foods contained very little seafood and the seafood that was part of dog food was included as a mix with chicken and/ or other ingredients. The more consistent levels of Se found in dog diets would suggest their ingredients (chicken, beef, other meats and vegetables) contain more similar levels of Se. Consequently normal dietary levels of Se found in commercially available canine diets were lower and less variable than those of found in feline diets.
Summary
The importance of Se in nutrition and health has been well documented in many species. Although there are limited data available relating to the function and importance of Se in companion animals, based on work from other species it is assumed that Se is an essential dietary requirement for cats and dogs. A review of the literature revealed the need for information relating specifically to the requirements of cats and dogs. To achieve this, an understanding of the optimum tissue Se levels, as well as those that result in toxicity and deficiency must be known. Furthermore, knowledge of Se metabolism, the availability of Se in pet food diets and the interactions of Se with other nutrients, is required to complete the picture of Se in companion animals.
Figure 3. Total selenium content of dog and cat foods categorised according to primary ingredient.
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Authors: S.E. SIMCOCK, S.M. RUTHERFURD and W.H. HENDRIKS
Institute of Food, Nutrition and Human Health, Massey University, Palmerston North, New Zealand
Author: S.E. SIMCOCK, S.M. RUTHERFURD AND W.H. HENDRIKS - Massey University (Courtesy of Alltech Inc.)
Publication date: 12/19/2006
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