Organic Selenium for Dairy Cattle

Selenium for Dairy Cattle: a Role for Organic Selenium

Published on: 10/26/2007
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Prior to establishment of the essentiality of selenium (Se) for animals by Schwarz and Foltz (1957), this element was considered primarily as a toxic element. The clinical signs of selenosis in livestock were primarily found in the US in South Dakota and northern Nebraska where animals grazed plants which had accumulated toxic levels of Se. The first reports of the effects of Se deficiency in ruminants are the studies with calves (Muth et al., 1957) and lambs (Hogue, 1958) demonstrating that Se prevented nutritional muscular dystrophy. Following these studies, there have been numerous studies showing the benefits of Se along with vitamin E in a number of health related aspects of dairy cattle and other species.

Research is still in progress to determine additional forms and functions of Se in biological systems. Another item for which there are some questions is the amount required by cattle. Currently, the National Research Council’s publications on nutritional recommendations differ greatly for beef and dairy cattle with 0.3 ppm recommended for all dairy animals and 0.1 ppm recommended for beef cattle. It would appear that a difference for lactating animals could be justified based on difference in milk yield but growing animals should be similar. Recommendations for dietary levels needed should also include some assumptions on the bioavailability of the dietary source or form of Se.


In the book, ‘The Role of Selenium in Nutrition’, Combs and Combs (1986) give an extensive review of all aspects of Se nutrition. In reviewing deficiency diseases of Se in cattle, they list nutritional muscular dystrophy, reproductive disorders in cows, cystic ovarian disease, Se-responsive unthriftiness, an anemia associated with the presence of Heinz bodies and a multifocal hepatic necrosis referred to as ‘sawdust liver’. Some of these conditions are also related to vitamin E dietary levels. The reproductive disorders include an increase in retained placenta, an increase in uterine infection following calving and a reduction in conception rate.

One very important problem not discussed by Combs and Combs (1986) but which has received extensive discussion by others is the importance of Se and(or) Se and vitamin E in immune response and the reduction in the incidence of mastitis. Ohio researchers (Smith et al., 1984; Harrison et al., 1984) have been the leaders in demonstrating the value of Se and vitamin E in the reduction of mastitis when cattle are properly supplemented with Se.

There are many other symptoms in other species which are influenced by Se nutrition. In addition, studies are continuing on the form and biological functions of Se. For example, Arthur et al. (1990) have shown a biochemical role for Se in type I thyroxine 5¢-deiodinase. Selenoprotein W has been shown (Yeh et al., 1997) to have a different distribution than glutathione peroxidase activity and may indicate a role for the form of Se in white muscle disease. It is therefore very likely that Se could play an important role in some functions of dairy cattle which have not been demonstrated by research. Arthur (1997) presented an excellent discussion on the possible role of Se in nonglutathione functions at last year’s Alltech Annual Symposium.


Setting dietary requirements based solely on the Se content of the diet is difficult to do because many factors affect the bioavailability of Se. Combs and Combs (1986) state that bioavailability varies with the form of the Se compound, feedstuffs vary with respect to bioavailability, and other dietary factors can either enhance or decrease availability. In reviewing bioavailability of supplemental Se sources, Henry and Ammerman (1995) report that the relative bioavailabilities for cattle are sodium selenite, 100; cobalt selenite, 105; selenomethionine, 245; and Se yeast, 290. They also point out that currently only sodium selenite and sodium selenate can be legally used as supplemental sources in the US.

Vitamin E is probably the dietary ingredient which has the most profound effect on dietary Se needs. The actions of Se and vitamin E are synergistic and many studies have demonstrated a reduction or elimination of deficiency symptoms where either compound is used.Weiss et al. (1997) showed that dairy cows fed high levels of vitamin E (up to 4,000 IU/day) were less likely to have clinical mastitis when fed only 0.1 mg/kg of Se than cows receiving 100 IU/day of supplemental vitamin E. Weiss et al. (1997) state that cows in Se deficient areas of the US require between 5 and 10 mg/day of supplemental Se (approximately 0.3 ppm for the average lactating cow or 0.6 ppm for the average dry cow) to maintain blood and plasma concentrations in the optimal range. Most of their studies use sodium selenite as the source of Se.

Because of the possible effects of chronic Se toxicity, many diets are not supplemented to an optimum level. Because acute selenosis results in diarrhea, respiratory distress and neurologic impairment (Blood et al., 1983) and chronic selenosis can result in ill thrift and lameness, oversupplementation must be avoided. In an interesting survey of 253 cow-calf operations in 18 states Dargatz and Ross (1996) reported that overall, based on blood Se concentrations, 7.8% of the samples were severely deficient and another 10.4% were considered marginally deficient. In the southeast, where deficiency was most prevalent, blood Se content was either severely or marginally deficient in 40.0% of the herds that supplemented the cattle with Se. It would appear that supplementation is not adequate for many herds. Based on this survey, the relatively low level of supplementation recommended for beef cattle (NRC, 1996) of 0.1 to 0.2 ppm may not be adequate. The NRC recommendation is for total dietary Se and not supplemental Se.


In dairy herds where blood levels of Se do not reach optimal levels even when 0.3 mg/kg of Se is supplied, either enhancing factors such as vitamin E or a more bioavailable source of Se such as Se yeast might be recommended if approved as a source of Se. In many dairy herds, this may be most critical during the dry period or the first few weeks of lactation when feed intake (dry matter intake as % of body weight) is lowest.
Mahan and Parrett (1996) compared sodium selenite with Se-enriched yeast (Sel-Plex 50, Alltech Inc.) as dietary Se sources for grower and finisher swine. Their data demonstrated higher retention and lower excretion for the Se-enriched yeast than for sodium selenite. In a similar study with dairy cattle, Fisher et al. (1995) compared sodium selenite with Se yeast. Each source was fed at a rate of 2.2 mg Se/head/day. The results were somewhat similar to the studies with swine. The yeast resulted in higher serum Se concentrations and milk Se was higher for the cows receiving the Se yeast.



Twenty Holstein cows in an early stage of lactation (prior to 120 days of lactation) were assigned to a 2 × 2 factorial arrangement of treatments with an additional negative control. The four treatments were Se yeast (Sel-Plex 50, Alltech Inc.) supplemented at levels to provide 0.15 ppm Se and 0.30 ppm Se and sodium selenite to provide supplemental Se at 0.15 ppm Se and 0.30 ppm Se. The basal diet did not have any supplemental Se.
The trial was conducted over a 12 week period. Prior to this study the cows were receiving a diet with 0.3 ppm supplemental Se as sodium selenite. During the first 2 weeks all animals received a basal diet with no supplemental Se. Blood and milk samples were collected at the end of this 2 week period to serve as base values. The next 10 weeks, all animals received the experimental diets containing the levels of supplemental Se listed above.

The diet fed to all cows was a total mixed ration consisting of 50% forage, 10% whole cottonseed, and 40% concentrate based on dry matter content. The forage was a 50:50 mixture of alfalfa silage and corn silage.

The concentrate mix is shown in Table 1. The Se was fed as a topdress with the morning feeding and was fed to maintain an equal intake of Se from both Se sources.

During the 10 week period, milk and blood samples were collected at the end of weeks 2, 6 and 10 for later analysis. Daily milk weights and feed intake were recorded and body weights were taken at biweekly intervals. Liver biopsy samples were taken at the end of the trial.

Milk samples were analyzed for milk fat, protein and somatic cell counts. In addition, defatted milk samples were analyzed for Se content. Fecal and urine ‘grab samples’ were taken at 2, 6 and 10 weeks of treatment period for later analysis of Se content.

Blood was collected and processed to provide samples for whole blood and plasma analysis of Se and glutathione peroxidase activity of whole blood samples. Liver samples were analyzed for Se content.


Table 2 presents the feed intake and milk production performance. The daily dry matter consumed by the yeast supplemented cows was 22.2 kg as compared with 20.8 kg for the selenite supplemented cows and this difference was statistically significant at the P<0.04 level. Differences in feed intake and milk yield were not expected and the reason for the significant difference in feed intake is not apparent. Milk composition was in a normal range for all treatments.

Milk Se at week 10 was affected by both level of Se and source of Se (Table 3). Since the interaction between level and source was not significant, the results could be interpreted to show an additive effect of level and source. Milk Se responded to source by 2 weeks and did not change significantly during the 10 week feeding period.

Blood samples were analyzed for plasma Se, whole blood Se and glutathione peroxidase activity. Whole blood Se is considered by many to be the best measure of bioavailability of Se for lactating animals. Whole blood Se showed both an effect of Se level as well as an effect of source. Bioavailability, based on whole blood Se, would indicate that Sel-Plex 50 has about twice the bioavailability of sodium selenite. Plasma Se showed the same trends as whole blood Se but was not as sensitive a measurement as whole blood Se. Glutathione peroxidase activity was not a good measure of Se status in the trial.

Excretion patterns of Se via both urine and feces showed a clear effect of Se level but did not show an effect of source of Se. However, the trend was for a little lower level of excretion for the Se yeast-supplemented animals.

Liver Se (Table 2) values were quite variable within treatment. As a result the rather large differences due to source were not statistically significant.

All the values reported are similar to previously reported Se values and the Se content of milk and tissue would be considered normal. The data support previous reports in that Se yeast has a higher bioavailability than sodium selenite as a dietary source of Se.


Se levels in natural feedstuffs are not adequate for optimum performance of dairy cattle in much of the US. While impaired immune response (susceptibility to mastitis) and reproductive problems are most frequently associated with Se deficiency, other problems can also occur. The dry period and early lactation period are the most likely to be deficient when supplemented as mg/kg of diet because of the relatively low intake of feed during these periods. Either the use of enhancing factors such as vitamin E or the use of more bioavailable sources of Se such as Se yeast may be needed when limits are set on the amount of Se which can be added to the diet.


Arthur, J.R. 1997. Non-glutathione peroxidase functions of Selenium. In: Proceedings of the 13th Annual Symposium on Biotechnology in the Feed Industry. (T.P. Lyons and K.A. Jacques, Eds) Nottingham University Press. Loughborough, Leics, UK. pp. 143–154.

Arthur, J.R., F. Nicole and G.J. Beckett. 1990. Hepatic iodothyronine 5¢-deiodinase: the role of Selenium. Biochem. J. 272:537.

Blood, D.C., O.M. Radostets and J.A. Henderson. 1983. Veterinary Medicine. Bailliere Tindall, London. Combs, G.F., Jr. and S.B.

Combs. 1986. The Role of Selenium in Nutrition. Academic Press, Inc., Orlando, Florida.

Dargatz, D.A. and P.F. Ross. 1996. Blood Selenium concentrations in cows and heifers on 253 cow-calf operations in 18 states. J. Anim. Sci. 74:2891.

Fisher, D.D., R.D. Elliott, S.W. Saxton and J.M. Beatty. 1995. Effects of Selenium source, Selenium status of lactating cows. Vet. Clin. Nutr. 2:68.

Harrison, J.H., D.D. Hancock, and H.R. Conrad. 1984.Vitamin E and Selenium for reproduction of the dairy cow. J. Dairy Sci. 67:123.

Henry, P.R. and C.B. Ammerman. 1995. Selenium Bioavailability. In: Bioavailability of Nutrients For Animals, Amino Acids, Minerals, and Vitamins. C.B. Ammerman, D.H. Baker, and A. J. Lewis (Eds.). Academic Press, New York.

Hogue, D.E. 1958. Vitamin E, Selenium and other factors related to nutritional muscular dystrophy in lambs. Proc. Cornell Nutr. Conf., Ithaca, NY. pp. 32–34.

Mahan, D.C. and N.A. Parrett. 1996. Evaluating the efficacy of Seleniumenriched yeast and sodium selenite on tissue Selenium retention and serum glutathione peroxidase activity in grower and finisher swine. J. Anim. Sci. 74:2967.

Muth, O.H., J.E. Oldfield, L.F. Remmert and J.R. Schubert. 1957. Effects of Selenium and vitamin E on white muscle disease. Science 128:1090.

National Research Council, 1989. Nutrient Requirements of Dairy Cattle. 6th revised ed. National Academy Press, Washington, DC.

National Research Council, 1996. Nutrient Requirements of Beef Cattle. 7th revised ed. National Academy Press, Washington, DC.

Schwarz, K. and C.M. Foltz. 1957. Se as an integral part of Factor 3 against dietary necrotic liver degeneration. J. Am. Chem. Soc. 79:3292.

Smith, K.L., J.H. Harrison, D.D. Hancock, D.A. Todhunter and H.R. Conrad. 1984. Effect of vitamin E and Selenium supplementation on incidence of clinical mastitis and duration of clinical symptoms. J. Dairy Sci. 67:1293.

Weiss, W.P., J.S. Hogan, D.A. Todhunter and K.L. Smith. 1997. Effect of vitamin E supplementation in diets with a low concentration of Selenium on mammary gland health of dairy cows. J. Dairy Sci. 80:1728.

Yeh, Jan-Ying, Qui-Ping Gu, M.A. Beilstein, N. E. Forsberg and P. D. Whanger. 1997. Selenium influences tissue levels of selenoproteinWin sheep. J. Nutr.

Department of Animal Science, University of Kentucky, Lexington, Kentucky, USA
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