By Steve Ensley, DVM, PhD, Veterinary Toxicologist and Mike Carlson, PhD, Analytical Chemist
The following discussion is directed primarily toward the beef cow, but does apply in general to other species, particularly where annotated. Reference values given for perinatal tissues are limited, and cannot be assumed to be he same as those given for older animals. Normal values for tissue elemental/micronutrient concentrations also differ considerably between species.
Copper and selenium are essential micronutrients for cattle and other food animal species. Copper deficiency can be manifested by poor growth rate, diarrhea, loss of hair color, infertility, abortion and "downer" cows. Most clinical signs reflect impairment of copper dependent or related enzyme systems. Clinical signs associated with selenium deficiency are often nonspecific. Degenerative myopathies, decreased thriftiness, increased placental retention, birth of premature or weak calves and a "owner cow" syndrome have been associated with selenium deficiency.
The liver is the principle site of copper accumulation and storage in the bovine fetus. Copper concentrations are greater than those seen in the adult bovine animal. Copper content in fetal liver may be uneven in distribution, with greatest concentrations reported in the caudate lobe.
No correlation appears to exist between maternal liver copper concentrations and accumulation of fetal hepatic copper until 180 days of gestation, when there is a gradual decrease in fetal liver content in copper deficient dams. Fetal liver concentrations from dams on adequate dietary copper tend to increase and not decline. In sheep, copper does not usually accumulate in fetal liver like in cattle.
Normally expected copper concentrations in bovine tissues (wet weight) are usually 4 to 6 ppm for kidney, 25 to 150 ppm for adult liver, 35 to 200 ppm for perinatal liver and 0.8 to 1.5 ppm for serum. Serum copper values alone are not consistently reliable indicators of Cu deficiency, since serum concentrations will be maintained at the expense of liver storage.
Copper concentrations of all bovine tissues except eye, tongue, skin, bone and liver are usually comparable in both fetus and adult. Copper concentrations in bovine tissues can vary with breed, soil composition, forages and degree and type of copper supplementation. High dietary nitrate content may depress copper utilization. Metabolism, availability, and toxicity of copper are also influenced by the presence of molybdenum, sulfur, manganese, zinc, iron and selenium.
Selenium is an important dietary micronutrient and is a component of the enzyme glutathione peroxidase GSH-Px, which protects cell membranes from oxidation by hydrogen peroxide and lipid peroxides. Selenium deficiency has been linked to white muscle disease (WMD), retained placenta and impaired immune response to infectious diseases. Selenium has the ability to cross the placenta in both cattle and sheep and be sequestered in the fetal liver even with low availability in the dam.
Normally expected selenium concentrations in bovine tissues (wet weight) are usually 0.25 to 0.50 ppm for liver, 1.0 to 1.5 ppm for kidney, 0.07 to 0.30 ppm for serum and > 0.10 ppm for whole blood. Fetal liver can contain up to twice the Se content of adult liver on a dry matter basis (fetal ppm wet weight X 6 = dry weight). A common finding in the vast majority of perinatal mortality cases (bovine) over the past several calving seasons has been well below expected Se values in perinatal kidney. The significance of this finding and the relationship to abortion etiology and pathophysiology is not completely understood at this time.
Evidence and analytical findings that low or deficient selenium can result in abortion are largely circumstantial, but cannot be ignored. The interrelationship of vitamin E and selenium must be considered when evaluating their significance in bovine abortion. Blood and tissue activity of GSH-Px is directly related to dietary selenium content. Selenium and vitamin E (alpha-tocopherol) have related roles protecting biological membranes and cells from oxidative degradation by peroxides. Vitamin E appears to be effective as a lipid-soluble antioxidant in the cell membrane, whereas selenium functions as a component of cytosolic GSH-Px to reduce peroxides. Less than adequate vitamin E or selenium can result in cellular membrane damage and reduced intracellular energy metabolism, either of which can impair cellular defense mechanisms. Both selenium and vitamin E have been shown to enhance the immunological competence of a number of domestic animal species. Also, without adequate vitamin E, a relative selenium deficiency could be manifested, even with adequate Se storage in the liver. The interrelationship between Se and vitamin E makes if difficult to distinguish between effects of deficiency in one of the other.
The vitamin E requirements of agricultural livestock may be influenced by a variety of factors. A high proportion of polyunsaturated fatty acids and deficiencies of Se and sulfur-containing amino acids may increase the vitamin E requirement considerably. In addition, stress and high dietary concentrations of nitrates, heavy metals or mycotoxins may increase the vitamin E requirement. Normally expected vitamin E concentrations in bovine tissues are usually 14-20 /µg/g (dry weight) for adult liver, 4 to 8 µg/g (dry weight) for fetal liver, 2 to 4 /µg/ml for adult serum and 0.2 to 0.4 µg/ml for fetal serum.
Cause and effect relationships of trace element aberrations with abortions and perinatal mortality have not yet been completely characterized, but suggest a nutritional/metabolic disorder in which excessive nitrate exposure, gestation and environmental stresses, and inadequate copper, selenium and other essential micronutrients may all be contributing factors.