Selenium deficiency in ruminants (Proceedings)


Selenium deficiency in ruminants (Proceedings)

Aug 01, 2009

The classic nutritional research of Schwarz and Foltz (1957), showing that selenium (Se) was the critical element in Factor 3 that prevented liver necrosis in rats, began the work that has subsequently proven Se to be an essential nutrient for man, cattle, other grazing ruminants, and all vertebrates examined to date. Subsequently, Muth (1963) and Hogue et al. (1962) reported that Se and vitamin E administration prevented white muscle disease in young ruminants. In recent years, several Se-responsive conditions have been described in cattle and these have been reviewed (Maas, 1983). The Se-responsive conditions in cattle include, nutritional myodegeneration (white muscle disease), retained placenta, abortions, neonatal weakness, diarrhea, ill-thrift, infertility, and immune system deficits. Minimum dietary requirements of cattle for Se were developed from feeding and response trials. In 1973, Rotruck et al. published work that outlined a basic biochemical mechanism that accounted for the role of Se as an essential nutrient. That work (Rotruck et al., 1973) showed that Se was a component of glutathione peroxidase (GSH-Px; E.C. in erythrocytes. It was later shown that GSH-Px contained 4 grams atoms of Se per mole of GSH-Px. For many years this was the only known biochemical role of Se, and while GSH-Px was found to have important antioxidant activity, it was recognized that several tissues had high Se concentrations and low GSH-Px activities. In addition to the original GSH-Px, now referred to as cellular glutathione peroxidase (cGSH-Px) three other glutathione peroxidases have been characterized (Ursini, Maiorino, and Gregolin, 1985; Takahashi, et al., 1987; Chu, Doroshow, and Esworthy, 1993). Both type I and type II iodothyronine deiodinases that contain Se have been characterized (Behne, et al., 1990; Arthur, Nicol, and Beckett, 1990; Berry, Banu, and Larsen, 1991; Croteau, et al., 1995). Additionally, three other selenoproteins have been sequenced and characterized, but their biological role is unknown (Hill, et al., 1991; Karimpour, et al., 1992). Recently, a new 18-kD membrane bound selenoprotein has been reported (Kyriakopoulos, et al., 1996). All the Se-containing proteins described contain selenocysteine and all appear to be genetically controlled. While the various biochemical and physiologic functions of all of these proteins is not presently clear, it is evident that Se is an important antioxidant and this helps to explain its role in prevention of a number of disease conditions. At the present time, the only clinical use of Se-containing enzymes is the analysis of blood GSH-Px activity for diagnosis of Se status by some laboratories.

Several disease syndromes in cattle have been shown to be Se-responsive; Se administration will reverse the condition or prior Se supplementation will prevent the condition. In the original work by Muth (1963), not all of the Se-deficient forages would produce white muscle disease, and while Se administration would successfully prevent or treat white muscle disease, it was apparent that factor(s) other than Se deficiency were involved. The other Se-responsive syndromes are similar in that Se deficiency is the underlying problem to be addressed, while other factors involved with pregnancy, infectious diseases, exercise, or stress are important for the condition to become manifest. The Se-responsive syndromes can be put into four major disease categories; (1) musculoskeletal, (2) reproductive, (3) gastrointestinal, and (4) immunologic.

The musculoskeletal conditions include nutritional myodegeneration (NMD; white muscle disease), neonatal weakness, and myodegeneration of adult cattle. These diseases, particularly NMD are widespread throughout the world and affects both domestic and wild ruminants. It is a particular problem in the U.S., Canada, Australia, New Zealand, and Europe. The cardiac form of NMD can occur within two to three days of birth and is often associated with severe myocardial lesions and peracute to acute death. Calves or lambs affected at one to four weeks of age often appear lame or stiff and are reluctant to move. Elevated serum enzymes of muscle origin such as creatinine kinase are helpful in diagnosing the myopathy. On post mortem examination, pale streaks are seen in the muscles. The cardiac form of NMD is more severe, with necrosis and calcification of the heart muscle and the intercostal muscles. Neonatal weakness due to Se deficiency is a less severe clinical manifestation. Myodegeneration of adult cattle is often associated with exercise or parturition, and common clinical signs include paresis and myoglobinuria. The role of Se as an antioxidant is a key factor in these musculoskeletal conditions. Grazing ruminants are particularly susceptible to Se deficiency diseases as their diets often consist of feeds from a small geographic area; if the soil and plants are low in Se in that area, animals are particularly predisposed.