Selenium and Vitamin E - Antioxidants for Animals

Larry L. Berger, Ph.D.
University of Illinois

“Antioxidants” have become a household word in the past few years.  Almost every checkout lane has one or more magazines with human nutrition articles describing the latest discovery concerning antioxidants.  Antioxidants have been associated with a reduced risk of cancer, cardiovascular disease, cataracts, and Alzheimer’s disease, as well as enhanced immune function and a slowing of the aging process.  Because the benefits of antioxidants have more to do with the prevention rather than the treatment of these diseases, large long-term studies are required to demonstrate their effectiveness.   Recent research suggest that the antioxidant status of livestock and other animals may also be important in improving health and longevity.  The purpose of this article is to review our current understanding of the role of antioxidants in livestock and other animals with special emphasis on selenium and vitamin E. 

Why Antioxidants?

Oxidation is a normal part of metabolism, like “combustion” in animals’ “internal combustion engine.”   Carbohydrates and fat are oxidized in the body to provide energy.  The immune system uses strong oxidizers to destroy invading organism.  Oxidation also occurs in nature continuously.  Rusting of iron is a common example.  So, why are antioxidants important? 

Free radicals are chemicals possessing an unpaired electron, which are usually very reactive.  They can be produced in healthy cells by accident or deliberately as with  phagocytosis in the immune system.  The most important free radicals in aerobic cells are oxygen and its derivatives (superoxide and hydroxyl radicals), hydrogen peroxide and transition metals.  If oxidizing compounds called free radicals are allowed to accumulate, they will damage or destroy cells in the body.  

Because most molecules maintain stability by having paired electrons, free radicals seek to steal electrons from other molecules.   Antioxidants are molecules that can easily and harmlessly give up an electron.  Nature produces an array of antioxidants to prevent free radical formation or to limit their damaging effects in cells.  These include enzymes to decompose peroxides, protein to bind transition metals, and other compounds that scavenge free radicals.  The most important biological antioxidants are vitamins A, C, E and selenium, a key component of glutathione peroxidase.  Vitamin A and or other carotenoids are abundant in many animal feeds and inexpensive to supplement.  Vitamin C is produced naturally in the tissues of farm animals and thus is not routinely supplemented.  Vitamin E is relatively expensive to add to diets.  Selenium is deficient in many feedstuffs grown in the Midwest which are then shipped throughout the US and exported.  Vitamin E and selenium play complementary roles as antioxidants and thus will be discussed together. 

Selenium-Vitamin E Team

Selenium is an essential component of the enzyme glutathione peroxidase.  Glutathione peroxidase is a major intracellular antioxidant that catalyzes the reduction of hydrogen peroxide and organic hydroperoxides to nontoxic compounds.  Vitamin E (alpha-tocopherol) is the major antioxidant in cell membranes.  Numerous experiments have demonstrated an antioxidant synergism between glutathione peroxidase (selenium) and vitamin E. 

The immune system is one example of where this synergism is most easily observed.  Wuryastuti (1993) studied the effects of vitamin E and selenium on immune responses in sows.  Phytohemagglutinin, canavalin A and pokeweed mitogen were used to determine whether peripheral blood lymphocytes were affected by selenium and vitamin E status.  Vitamin E deficient sows had a significantly low immune response to these mitogens.  However, when both selenium and vitamin E were deficient, impairment of mitogenic stimulation occurred even earlier, compared to those sows that were only deficient in vitamin E.  These data suggest that optimum immune response required adequate levels of both selenium and vitamin E.  Nockels ( 1991) noted similar effects in cattle in that antibody titers were greater when both selenium and vitamin E were supplemented.  In this same review, it was reported that selenium and vitamin E independently increased antibody titers in sheep exposed to the para-influenza₃ virus.  

Oxidative stress may be the link that explains the interactions between animals stress, nutritional deficiencies and decreased disease resistance often observed in the field (Spurlin and Spain, 1999).  In cattle, the production of reactive oxygen metabolites can be increased by the consumption of Maillard reaction products, mycotoxins, and endophyte-infected tall fescue.  Unbound or “ill-place” iron can increase the production of reactive oxygen metabolites.   Miller et al. (1993) showed that inflammation, infections and environmental stresses may encourage the formation of ill-placed iron.   Under these conditions the need for antioxidants is increased.  If animals are marginally deficient in selenium and/or vitamin E, the responsiveness of their immune system is impaired.  These animals are more likely to become diseased and or die, while animals with a strong immune system may show no symptoms. 

In the past few years there has been an effort to increase the energy density of animal diets.  With calorie-dense diets animal performance is maximized, feed efficiency is improved and less animal waste is generated.  Fats additions are a common means of increasing caloric density.  However, recent data suggest that adding certain types of fat can increase the requirements for antioxidants. If not met the oxidant deficiency may increase an animal’s susceptibility to disease.   

Beck et al (1994) conducted a study in mice where the diets were supplemented with lard (saturated fat) or menhaden fish oil (unsaturated oil).   The diets were supplemented with 0.2 ppm selenium and 38.4 mg/kg of d-alpha tocopheryl actate.   These levels of selenium and vitamin E are considered adequate for mice, but are not supernutritional levels.  Diets that were deficient in vitamin E, selenium, or both were also fed. After being fed the test diets for four weeks the mice were exposed to a virus that causes lesions in the heart.  Both selenium and vitamin E deficiency increased the cardiac muscle damage.  However, the most severe lesions were seen in mice fed the menhaden fish oil diets deficient in both selenium and vitamin E.  No lesions were observed in mice fed diets that were adequate in selenium and vitamin E.  Unsaturated fatty acids like those in fish oil increase the need for antioxidants in the diet.  When animals are in a “marginal antioxidant status” the type of fat source added to the diet may affect an animal’s susceptibility to disease.  

Large-scale animal production units are constantly seeking ways to minimize stress and enhance immune function.  Antibiotic feeding has been used in many production settings to control subclinical diseases.  Although this has been effective in the past, and the real dangers of continued use are still controversial, it is likely that this practice will become increasingly regulated in the future.  Consequently, maximizing the immune status of the animal is critical to optimum health and longevity.  Antioxidant concentrations in the diet, especially selenium and vitamin E, will receive increasing emphasis.   Feeding a trace mineralized salt and vitamin premix that have been properly fortified with selenium and vitamin E, respectively is essential to maintaining animal health and productivity.  

Literature Cited 

Beck, M.A., P.C. Kolbeck, L.H. Rohr, Qing Shi, V.C. Morris, and O. A. Levander. 1994. Vitamin E deficiency intensifies the myocardial injury of Coxsackie B3 infection of mice. U. Nutr. 124:345. 

Miller, J.K., E. Brezezinska-Selbodzinska, and F.C. Madsen. 1993. Oxidative stress, antioxidants, and animal function. J. Dairy Sci. 76:2812.  

Nockels, C.F., 1991.  If immunity fails, don’t pick on your drug salesman – it may be nutritional. Proc. The Range Beef Cow Symposium XII, Fort Collins, CO. p. 239. 

Spurlin, K.M., and J. Spain. 1999. Nutrition and immune function. Proc. AFIA Nutrition Council:  Interrelationship between nutrition and disease. St. Louis, MO. P. 16.