Observations on the efficacy of various forms of selenium for livestock: a review.

Since 1957, selenium has found extensive use in livestock production to maintain an adequate selenium status in animals in areas of soil and feed/forage deficiency. Selenium may be given directly to livestock, or applied as a fertilizer amendment to increase selenium content of their feeds. This paper addresses the area of direct supplementation, which includes oral and parenteral supplementation, and with ruminant animals the use of slow-release boluses. Various chemical forms of selenium have been examined as supplemental sources, with sodium selenite being the earliest compound of choice. Combination of selenium supplementation with other livestock management practices led to use of selenium dioxide, which avoided solubility problems with selenite but produced effective responses. Barium salts have been used with some success as supplemental selenium sources. Experience with ruminal boluses has shown that high pressure pelleting of increased grain size selenium, in hollow pellets, has prolonged their useful life. Attention has been paid recently to residual selenium returned to the soil from livestock supplementation practices and the resulting opinion is that currently approved practices are acceptable from the point of view of environmental quality.

Oxytocin synthesis and secretion from bovine corpora lutea exposed in vitro to cycloheximide and colchicine.

Two experiments were conducted to study the effects of cycloheximide and colchicine on prostaglandin F2 alpha (PGF2 alpha)-induced secretion and synthesis of oxytocin in bovine luteal tissue in vitro. Corpora lutea were collected from beef heifers on Day 8 of the estrous cycle. In Experiment 1, incorporation of [14C]-leucine into oxytocin synthesized and secreted by luteal slices after exposure to PGF2 alpha, cycloheximide and cycloheximide plus PGF2 alpha was examined. In Experiment 2, synthesis and secretion of oxytocin were evaluated in luteal slices incubated with colchicine and PGF2 alpha alone and in combination. Cycloheximide inhibited incorporation of labeled leucine into luteal proteins by more than 90% and no labeled oxytocin was detected in the media or tissue. Prostaglandin F2 alpha induced significant secretion of oxytocin that was not inhibited by cycloheximide. Tissue levels of oxytocin after incubation with cycloheximide and/or PGF2 alpha did not differ and were similar to those of the incubated control. Colchicine alone did not suppress oxytocin secretion and did not alter the ability of PGF2 alpha to induce significant secretion of this nonapeptide. Tissue concentrations of oxytocin after incubation with colchicine and/or PGF2 alpha did not differ. These studies indicate that secretion and replenishment of luteal oxytocin in vitro is not contingent upon de novo protein synthesis. Inability of colchicine to suppress oxytocin secretion and synthesis may have been due to the short duration of exposure of luteal tissue to the drug.

Risks and benefits in agricultural uses of selenium.

Selenium deficiency in soils, and subsequently in crops that are grown on them, has been charted in various parts of the world. Use of carefully regulated amounts of supplemental selenium in such areas has been effective in improving productive performance of domestic food-producing animals, and some 30 years' experience has now been gained with various supplementation practices. Coincidentaliy, there have been instances reported of situations where selenium toxicity has resulted from a combination of naturally-high environmental levels, enhanced by agricultural, environmental and industrial practices, and questions have been raised as to whether continued animal supplementation may contribute to selenium toxicity. This paper examines some of the various factors involved and concludes that presently-established animal supplementation uses of selenium are small compared with other sources of the element and that they do not constitute a hazard to animals, including humans, or the environment.

Selenium in animal nutrition: the Oregon and San Joaquin Valley (California) experiences--examples of correctable deficiencies in livestock.

White muscle disease and other selenium deficiency syndromes, once extremely common in young calves and lambs in Oregon, especially in the areas of volcanic origin east of the Cascade mountain range, prompted extensive investigations in the Oregon Agricultural Experiment Station that resulted in the implementation of large-scale selenium supplementation programs. Although selenium deficiency in livestock is consequently now rare in Oregon, selenium-deficient soils and attendant selenium deficiency conditions have been reported near the Kesterson Wildlife Refuge in the Northern part of the San Joaquin Valley, California, where, paradoxically, selenium toxicity in wildfowl, nesting near evaporation ponds, occurred and attracted wide attention. This review cites studies which explain why there is no evidence of selenium toxicity in livestock, but some selenium deficiency on the east side of the San Joaquin Valley. They also show that there is no threat to the food supply owing to excessive selenium in this area and that the consumption of meat and milk from the herds would not exceed the safe range of selenium for humans.

The two faces of selenium.

The nutritionally important trace elements share a high biological activity, implemented through association with enzymes, hormones or vitamins. The same activity responsible for physiological responses at extremely low dietary levels implies the potential for metabolic upset when the elements are ingested at elevated, although still relatively low levels. Selenium provides a classic example of this dichotomy of effects and has generated concerns at both ends of its supply spectrum. Experiences in the Dakotas, mid-19th century, led to identification of toxicity symptoms for which selenium was later shown to be responsible, while separate studies showed that excess selenium was teratogenic in the developing avian fetus. These toxic reactions suggested that selenium might be useful in restricting abnormal cell growth, and recent studies have proved it to be anticarcinogenic in certain specific circumstances. Investigation of selenium's nutrient function has been equally interesting, and when Schwarz showed it to be an essential nutrient in 1957, he began an era of intense research activity. Dietary levels of selenium below 0.02 ppm were found to cause deficiency symptoms affecting muscles, liver and pancreas and glutathione peroxidase was shown to be an active form through which selenium acted to prevent such aberrations. Research continues to seek other active organic combinations for selenium to identify interfering compounds that restrict its bioactivity and to explore biochemical mechanisms involved in its toxicity.

Prostaglandin F2 alpha-induced release of oxytocin from bovine corpora lutea in vitro.

Two experiments were conducted to study the in vitro effects of prostaglandins F2 alpha (PGF2 alpha), E2 (PGE2), and luteinizing hormone (LH) on oxytocin (OT) release from bovine luteal tissue. Luteal concentration of OT at different stages of the estrous cycle was also determined. In Experiment 1, sixteen beef heifers were assigned randomly in equal numbers (N = 4) to be killed on Days 4, 8, 12, and 16 of the estrous cycle (Day 0 = day of estrus). Corpora lutea were collected, an aliquot of each was removed for determination of initial OT concentration, and the remainder was sliced and incubated with vehicle (control) or with PGF2 alpha (10 ng/ml), PGE2 (10 ng/ml), or LH (5 ng/ml). Luteal tissue from heifers on Day 4 was sufficient only for determination of initial OT levels. Luteal OT concentrations (ng/g) increased from 414 +/- 84 on Day 4 to 2019 +/- 330 on Day 8 and then declined to 589 +/- 101 on Day 12 and 81 +/- 5 on Day 16. Prostaglandin F2 alpha induced a significant in vitro release of luteal OT (ng.g-1.2h-1) on Day 8 (2257 +/- 167 vs. control 1702 +/- 126) but not on Days 12 or 16 of the cycle. Prostaglandin E2 and LH did not affect OT release at any stage of the cycle studied. In Experiment 2, six heifers were used to investigate the in vitro dose-response relationship of 10, 20, and 40 ng PGF2 alpha/ml of medium on OT release from Day 8 luteal tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in serum prolactin concentrations and ovarian prolactin receptors during embryonic diapause in mink.

Experiments were conducted to determine if prolactin receptors were present in the mink ovary, and to examine the relationship between receptor numbers and serum levels of prolactin (PRL) during embryonic diapause and blastocyst reactivation. For analysis of the physicochemical properties of prolactin receptors, ovaries were obtained from anestrous mink. All binding determinations were made using 125I-ovine prolactin (125I-oPRL), and 20 micrograms of tissue protein from the 100,000 X g particulate fraction. To quantify prolactin receptors during gestation, 20 primiparous mink were mated twice on consecutive days between 4 and 10 March and assigned randomly to one of two groups. Mink in Group 1 (N=8) were killed on 13 March when blastocysts were completing their migration into the uterus and entering a state of diapause. Animals in Group 2 (N=10) were killed on 26 March during the period of blastocyst reactivation, just prior to implantation. To determine serum levels of prolactin during gestation, an additional 20 primiparous mink were similarly mated and bled every 4 days from 15 March to 8 April, and then every 7 days until 23 April. Prolactin concentrations were determined by a heterologous double antibody radioimmunoassay using porcine PRL for both tracer and standards. Optimum conditions for binding 125I-oPRL to ovarian membranes were attained at 25 degrees C after 12 h. Scatchard analysis revealed a single class of high affinity binding sites with a Kd of 6.14 X 10(-11) M. The total concentration of receptors during anestrus was 85 fmol/mg protein, which increased significantly during embryonic diapause to 484 fmol/mg protein, then declined to 16 fmol/mg during blastocyst reactivation.

Influence of copper supplementation on blood and liver copper in cattle fed tall fescue or quackgrass.

Copper concentrations were measured in naturally Cu-deficient and Cu-supplemented yearling Hereford heifers fed tall fescue (Festuca arundinacea Schreb.) or quackgrass (Agropyron repens [L] Beauv.) forage. The data were used to establish a relationship between dietary Cu supplementation and accumulation of liver Cu, and to test the influence of diet and Cu supplementation on blood plasma Cu and ceruloplasmin oxidase activity. Dietary Cu supplementation was positively correlated with accumulation of liver Cu; the rate of increase in liver Cu levels diminished at high supplementation rates (liver Cu = 410.43 - 353.47 x e-.00295 x mg Cu supplement; R2 = .740), suggesting an efficient mechanism preventing fast, toxic Cu-overloading in cattle. The linear relationship (R2 = .7878) between blood plasma Cu and ceruloplasmin oxidase activity indicated that similar percentages of blood plasma Cu were present as ceruloplasmin in deficient, normal and Cu-supplemented cattle. However, the portion of plasma Cu occurring as ceruloplasmin changes significantly with type of feed. When compared with quackgrass, tall fescue not only produced rapid Cu depletion in unsupplemented cattle, but affected intermediary Cy metabolism and activity of Cu-enzyme ceruloplasmin differently at all levels of experimental Cu supplementation.

Interaction of molybdenum, sulfate and alfalfa in the bovine.

Thirty-two weanling Hereford heifers were assigned to treatments in a 2(3) factorial arrangement involving two levels of Mo (0 and 100 ppm added inorganic Mo), two levels of SO4 (0 and .5% added inorganic SO4) and two levels of alfalfa pellets (0 and 2.72 kg daily). A basal diet of hay and salt ad libitum and 454 g milo pellets (92% milo and 8% molasses) was fed daily. All animals were fed individually for 11 mo. Added dietary Mo created severe symptoms of Mo toxicity that included scouring, achromotrichia, anemia and weight loss. Five of the 16 animals that received Mo died within 2 wk after the study was terminated. Molybdenum accumulated in all tissues sampled during the first 8 mo and decreased thereafter. Molybdenum also elevated plasma Cu. Balance data indicated that 100 ppm of added dietary Mo led to daily retention of 105 mg Mo and reduced the rate of liver Cu depreciation. Added Mo did not influence feed intake, digestibility or metabolizable energy (ME) when calculated per unit of metabolic size. Added inorganic SO4 lowered plasma Cu and Mo, but did not alter digestibility, ME or Cu and Mo balance. Added protein supplied by alfalfa pellets increased feed intake and digestibility of dry matter, crude protein and energy but did not prevent Mo toxicity symptoms. Alfalfa also increased ME, P, S and N balance and was involved with certain interactions with both Mo and SO4. Plasma Mo is a good indicator of Mo intake and is more useful than tissue Cu levels. Urinary Mo may also be useful to evaluate Mo intake under field conditions.

Prolactin binding sites in the uterus of the mink.

The present study was conducted to determine if specific binding sites for prolactin (PRL) are present in the uterus of the mink. Uteri of anestrous mink were homogenized and subjected to differential centrifugation into three particulate fractions, 1500, 15 000 and 50 000 X g. Binding of [125I]oPRL to membranes in an aliquot (200-400 micrograms protein) of the 50 000 X g particulate fraction was quantified. Time and temperature for optimal binding were 18 h at 25 degrees C. Scatchard plot analysis revealed a single set of binding sites for PRL with a Kd of 8.25 X 10(-11) +/- 0.68 M. The maximum amount of [125I]oPRL bound was 28 fmoles/mg protein. Prolactin binding sites were detected in both the uterus and kidney of mink, but not in skeletal muscle, spleen, diaphragm or lung. These data indicate that uterine cell membranes of the mink contain sites that bind prolactin with high affinity.

Photoperiodic effects on serum glucocorticoids and fur growth in mink.

The relationship of glucocorticoid secretion to artificial light-induced, early winter priming of pelage in ranch mink was investigated. On December 13, 1977, 16 mature female mink were exposed to natural light. On June 26, 1978, the animals were assigned randomly to one of two groups. Animals in Group 1 were housed in a light-control facility and subjected to 6 hr of artificial light daily and ambient temperatures until November 27, 1978. Animals in Group 2 served as controls and were exposed to natural light. Samples of blood and measurements of the fur and vulva were taken biweekly throughout the year. Concentrations of total glucocorticoids in serum were determined by competitive protein-binding assay. The pelage of mink reared under reduced artificial light was fully prime by October 31, while that of control animals did not become prime until November 27 (time x light regimen interaction, P less than .05). A seasonal effect (P less than .01) on total glucocorticoid concentrations in serum of control mink was revealed by a pattern of three peaks over the 12-month period. The pattern of glucocorticoid secretion was not affected by exposure of mink to reduced artificial light. Maximum concentrations of total glucocorticoids in serum occurred on the same date (September 5) in both groups, although levels were significantly higher in the light-treated mink (44.5 +/- 10.4 ng/ml) than in the controls 26.9 +/- 5.7 ng/ml). Fur growth was positively correlated with total glucocorticoid concentrations in serum during the period from June to December (overall r = .14, P less than .05). Both length and width of the vulva increased (P less than .01) during February and March in animals reared under natural light. These data suggest that the increased secretion of glucocorticoids induced by exposure of mink to reduced artificial light may be involved in promoting early priming of the winter pelage of these animals.

Biotin deficiency in mink fed spray-dried eggs.

Young standard dark mink developed classical symptoms of biotin deficiency, including underfur-greying, "spectacle eye," loss of fur, exudates from eyes, nose and mouth and encrustation of paws, when fed a diet containing 10% commercially produced, denatured spray-dried eggs. Comparable animals fed 5% spray-dried eggs did not show these symptoms; however, their pelts tended to be browner (i.e., lighter colored), than those of control animals. The feeding period during which these symptoms developed covered about 4 1/2 months: August 1 to December 13. Supplemental biotin (1.34 and .45 mg d-biotin per kilogram dry feed) prevented deficiency symptoms in mink fed 10% spray-dried egg of 20% fresh frozen whole chicken eggs, respectively. Eye exudates were most severe in October, when the combined stress of body and fur growth was greatest, then showed a partial remission as peak growth of body tissue and fur was passed. It was concluded that spray-dried eggs are insufficiently heat-treated to render their avidin content inactive; thus they should be appropriately supplemented with biotin for use in mink diets.

Effects of selenium and vitamin E deficiencies on reproduction, growth, blood components, and tissue lesions in sheep fed purified diets.

Three 2 X 2 factorial experiments were conducted with sheep fed purified diets to determine the effects of selenium and vitamin E on the incidence of white muscle disease (WMD) and blood components. All lambs reaching 6 weeks of age in the group receiving no vitamin E or selenium developed WMD lesions, whereas only a few lambs in either the +E - Se or -E + Se treatment groups developed these lesions. Plasma activities of creatine phosphokinase, lactic dehydrogenase and glutamic oxaloacetic transaminase were significantly elevated in lambs receiving no vitamin E or selenium, whereas these enzyme activities in those receiving only selenium were non-significantly elevated. The enzyme activities in plasma of those on the +E - Se or +E + Se treatments were maintained at low levels, suggesting vitamin E alone is more effective in preventing WMD than selenium alone. The metabolic interactions of these essentials are discussed.