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Biomedical subjects

J L Shupe

Publications and source records attributed to J L Shupe.

At least 19 recordsLinked to original sources

The pathology of chronic bovine fluorosis: a review.

Clinical, pathologic, and analytical records from 200 cattle were reviewed to determine if long-term exposures to elevated fluorides resulted in previously unrecognized or unreported pathologic changes, especially skeletal neoplasia. Animals were part of comprehensive field and laboratory investigations of bovine fluorosis conducted by the Utah State University Agricultural Experiment Station over a 25-year period. Records indicated that over 170 cattle included in this review were exposed to dietary fluorides levels in excess of 25 ppm (dry wt), for most of their life span, and these animals exhibited bone fluoride concentrations ranging between 2,000 and 12,500 ppm (dry wt). Although dental and/or skeletal changes were present in most animals, significant soft tissue damage or neoplasia was not observed in any organ system. Renal degeneration and mineralization were slightly more prevalent in range cattle ingesting high fluoride levels, but these changes were not recognized in animals that received high experimental fluoride doses. The absence of significant soft tissue damage or neoplasia in these cattle combined with results of an extensive literature review suggests that environmental fluorides are not significant factors in mammalian carcinogenesis.

Animals↗

Placental transfer of fluoride in Holstein cows.

Placental transfer of fluoride was studied in 40 Holstein cows and related to a previous 7 1/2 y study for comparative purposes. Animals were randomly assigned to fluoride dosage groups of control, 0.51, 1.31 or 2.66 sodium fluoride/d (10, 25, 50 or 100 ug/g feed). Each animal received the dose daily via gelatin bolus for 4-14 d prior to parturition. Maternal heparinized blood samples were collected before dosing and after parturition. Placental cotyledon and calf blood samples were collected from each animal immediately after parturition. Maternal and calf plasma and placental cotyledon fluorine concentrations were determined. Increased levels of fluoride given to pregnant cows resulted in significantly increased (p less than 0.05) maternal plasma and placental cotyledon fluorine concentrations. Calf plasma fluorine concentrations at birth did not significantly increase in relation to the fluoride treatment level of dams. The data support the concept that under normal circumstances in cattle there is a partial placental barrier to fluoride that operates to limit fluoride concentrations in the fetal circulation and tissues.

Animals↗

DNA polymorphism analysis of hereditary multiple exostoses in horses.

Genomic DNA polymorphisms obtained by restriction fragment-length polymorphism from healthy horses and horses with hereditary multiple exostoses were analyzed. These DNA were digested by 12 restriction enzymes and were hybridized against 6 isotopically labeled oncogene probes. Hybridization was not detected with the viral oncogene, v-ras, which indicated this oncogene was absent in the equine genome. Oncogenes (c-raf-1, c-fes, c-myb, c-myc, and c-sis) were present and had similar hybridization patterns and signal intensities in DNA from healthy horses and horses with hereditary multiple exostoses. Unique and distinct restriction fragment-length polymorphisms were detected with the c-raf-1 probe only in BamHI- and PstI-digested equine DNA.

Animals↗

Clinical signs and bone changes associated with phosphorus deficiency in beef cattle.

For 10 years, 42 female Herefords (as they progressed from weanling calves to aged cows) were fed diets individually, with phosphorus (P) content being the only variable. During growth and the first 3 gestations, clinically evident differences were not associated with 2 dietary treatments (approx 12 and 38 g of P/day). During the next 2 gestations (2 years), half the cows from each original treatment group were fed less than 6 g of P (n = 21 cows, 11 from the group fed 12 g of P/day and 10 from the group fed 38 g of P/day) daily. The other half were fed diets supplying approximately 8 g of P (n = 11 cows fed 12 g of P/day) and 35 g of P (n = 10 cows fed 38 g of P/day) daily. During the last 3 years of the experiment, all remaining cows were fed diets containing 12 g (n = 19 cows originally fed 12 g) or 19 g (n = 17 cows originally fed 38 g) of P/day. Cows fed diets containing less than 6 g of P/day developed an insidious and subtle complex syndrome characterized by weight loss, rough hair coat, abnormal stance, and lameness. Spontaneous fractures occurred in the vertebrae, pelvis, and ribs. In severely affected cows, fractures did not heal properly. Some bones were demineralized markedly, and the cortical surfaces were porous, chalky white, soft, and fragile. Osteoid tissue was not properly mineralized. Radiography revealed diminished bone density (osteoporosis), cortical thinning, and resorption of trabeculae. Time-related availability of dietary P initiated excessive turnover of bone, with resultant structural changes and impaired function.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of diets containing sodium fluoride on mink.

Mink (Mustela vison) kits still nursing, and adult male mink were fed diets containing various levels of fluorine (as NaF) to determine the effects on health, growth and pelt quality. Different groups were fed diets containing 25.5 (control), 46.0, 111.5 or 287.0 ppm fluorine (on a wet basis) for 7-8 mo. Gross, radiographic and microscopic changes were seen in bones from some animals ingesting the higher levels of fluorine. Chemical analyses for fluorine generally reflected levels ingested. Fluorine caused no detectable differences in pelt quality. After data were evaluated, tolerance levels in the feed of not more than 50 ppm fluorine for breeding stock and 100 ppm fluorine for animals being raised only for pelts are recommended.

Animals↗

Relationship of cheek tooth abrasion to fluoride-induced permanent incisor lesions in livestock.

Teeth from cattle, sheep, and horses that ingested various fluoride intakes and teeth from field studies of these species plus deer, elk, and bison were examined for abnormalities. Approximately 99,000 animals in 322 herds were examined for fluorosis. From field studies, 988 cattle of various ages and with different degrees of dental fluorosis were slaughtered and necropsied. The severity of fluoride-induced mottling, hypoplasia, and abnormal abrasion of paired permanent incisor teeth was correlated with abrasion of premolar and molar (cheek) teeth that form and mineralize at approximately the same age. Severe irregular wear of cheek teeth impaired mastication and resulted in poor utilization of feed and unthriftiness. Excessive amounts of fluoride during tooth formation and mineralization induce characteristic dental changes. Offspring from the fluoride-affected animals did not have discernible fluoride-induced lesions in the deciduous teeth.

Animals↗

Clinical effects of low dietary phosphorus concentrations in feed given to lactating dairy cows.

Thirty-four Holstein cows, pregnant with their second calf, were individually fed diets containing 3 concentrations of phosphorus (P): 24 cows for 12 months and 10 cows for 7.5 months of lactation. Cows were randomly allotted to the specific dietary groups 2 months before expected parturition. The 3 dietary concentrations of P were 0.24%, 0.32%, and 0.42% in diet. Cows given 0.24% P in diets produced significantly less milk than did cows in the other groups. Other clinical signs of P deficiency in the cows fed the diet with 0.24% P included loss of body weight, decreased feed consumption, and lower inorganic serum P concentration 2 to 10 weeks after parturition. There were no significant differences in the variables measured between cows given dietary P concentrations of 0.32% and 0.42%. There was no evidence of hemoglobinuria after parturition. Reproductive performance did not differ significantly, although the trend was in favor of the cows fed the diet with 0.24% P.

Animals↗

Dietary phosphorus for beef cows.

Hereford heifers (48 initially) were individually fed variable amounts of dietary phosphorus (P) from weaning through their 8th gestation. During phase I, 2 groups (24 cows each) were given 20.6 to 38.1 g of P/day and 6.0 to 12.1 g of P/day (increasing as animals grew). During phase II (the 4th gestation), half of the animals from each group were maintained with the same respective diets, and the other half were given 5.1 to 6.6 g of P/day. Within 6 months, animals given 5.1 to 6.6 g of P/day gradually developed signs of P deficiency. Clinical signs of deficiency and lesions included general unthriftiness, body weight loss, reduced feed consumption, reluctance to move, abnormal stance, spontaneous bone fractures, and finally, impaired reproductive performance. Cows given 7.8 to 8.9 g of P/day in diet 2 during phase II did not develop discernible clinical signs of P deficiency. Cows that were given 5.1 to 6.6 g of P/day apparently regained their health and reproductive capability when fed 11.7 to 12.6 or 17.1 to 20.5 g of P/day. The data indicate that bones serve as an effective storage source of P and support and buffer body needs until there is serious depletion of skeletal P. These results indicate that common recommendations for dietary P, such as those outlined by the National Research Council (17.5 g of P/day over the entire year for cows weighing 450 kg), exceed the basic requirements for beef cattle; 12 g of P/day is adequate for 450-kg beef cows.

Animals↗

Short term disposition of soluble vs. insoluble forms of cadmium in rat lung after intratracheal administration: an autoradiographic assessment.

An autoradiographic study was undertaken to compare the initial distribution patterns of soluble and less soluble forms of cadmium in the rat lung after intratracheal (i.t.) instillation. Male Sprague--Dawley rats were divided into 2 groups, each group received either soluble or a less soluble cadmium (109Cd) i.t. in 0.1 ml buffered saline. At 5, 30 and 90 min post-instillation, rats were sacrificed and processed for autoradiography, and radioactivity estimation of lung sections. 109Cd was unevenly distributed in the lungs at 5 min for both forms of Cd. At 90 min post-instillation, 109Cd was almost evenly distributed in the lung instilled with the soluble form; in case of the less soluble form a spotty distribution of 109Cd in the bronchi was observed. 109Cd was mainly translocated to the liver and stomach, followed by the kidney and intestine. It is apparent that the initial translocation of instilled 109Cd from the lung is relatively slow in the case of less soluble form as compared with the soluble form.

Animals↗

Fluoride toxicosis in wild ungulates.

To compare the occurrence of chronic fluoride toxicosis in wild and domestic animals in selected areas of Utah, Idaho, Montana, and Wyoming, deer, elk, and bison bones and teeth were collected for evaluation. Vegetation and drinking water samples also were collected, so that potential sources of fluoride could be evaluated. Deer, elk, and bison were found to be susceptible to the adverse effects of ingestion of excessive amounts of fluoride. Teeth and bones were primarily affected with characteristic lesions. Pathognomonic soft tissue changes were not observed. The animals had been exposed to a variety of sources of excessive fluoride, including water high in fluoride, forages contaminated by industrial effluents that were high in fluoride, vegetation contaminated with high fluoride-content soil by rain splash or wind, or a combination of these sources. Waters high in fluoride, especially from geothermal springs and wells, often contained appreciable amounts of various soluble salts. Evidence accumulated from specimens collected throughout the aforementioned states indicated that there are areas where chronic fluoride toxicosis is a problem for wildlife. These areas were where natural sources of fluorine (especially geothermal waters) provided amounts for ingestion that exceed species tolerance limits or were near certain industrial operations.

Animals↗

Teratogenic plants.

Abnormal, defective offspring are a significant problem in livestock as well as in humans. Congenital malformations have been observed since ancient times and were once thought to be primarily of genetic origin. Knowledge relating to congenital anomalies has greatly increased in recent years. Numerous hazardous plants are abundant on many of the ranges grazed by livestock. Many of the plants, when ingested during certain stages of gestation, induce congenital defects. The defects can vary from minor changes to striking abnormalities. The final manifestations of abnormal intrauterine differentiation and development are death, resulting in reabsorption or abortion, malformation, suppression of growth, and disordered function. It appears that the type of malformation induced in a conceptus depends more upon the developmental stages in which the injurious agent operates than upon the type of the agent. The etiology and pathogenesis of congenital defects are complex. With time, and additional studies, other plants will probably prove to be teratogenic. Teratogenic studies and findings in animals have had beneficial influences for the livestock industry and for veterinary and human medicine.

Animals↗

Accumulation and depletion of cadmium and lead in tissues and milk of lactating cows fed small amounts of these metals.

Groups of lactating cows were fed 0, 40, and 200 mg of added cadmium (as chloride) and 0, 100, and 500 mg of added lead (as acetate) per animal per day in separate experiments. Milk and blood were sampled periodically and analyzed for concentrations of metal ions. Metal feeding was discontinued after 3 mo, and selected animals were necropsied for tissue residue studies. Remaining animals were continued on control ration for another 3 mo and then killed and tissues obtained. Cadmium feeding did not produce a dose-related increase of this metal in blood, milk, or skeletal muscle. Liver and kidneys were the primary organs of cadmium accumulation, and concentration of cadmium in these organs continued to rise during 3 mo of feeding the control diet after the initial exposure period. Lead did not accumulate in skeletal muscle but showed a dose-related increase in blood, milk, bone, liver, and kidney. In most tissues there was a rapid decline of lead concentrations after cessation of treatment, except in bone. Low dietary intake of cadmium and lead do not produce an appreciable rise of these metals in edible products, e.g., milk or meat. Of the tissues analyzed, liver and kidney accumulate both cadmium and lead, and cadmium especially persists in these organs for long periods. Bone is the primary site of deposition for lead but not cadmium.

Animals↗

Effect of excessive exposure to sodium fluoride on composition and crystallinity of equine bone tumors.

Sodium fluoride (5 mg/kg of body weight) was fed for 20 months to horses with hereditary multiple exostoses (HME), a skeletal disorder that primarily affects endochondral bones during skeletal development. Rib biopsies were performed on both HME horses not fed fluoride (control) and HME horses that were fed fluoride to obtain comparable specimens for chemical analyses and x-ray diffraction. Fluoride content of the rib from a horse fed fluoride for 20 months was approximately 20 to 30 times higher than that from a control horse. Fluoride content of the bone tumors was higher than those of normal bones in both control and fluoride-fed horses. The effect of fluoride uptake on the Ca/P ratio was slight. The Ca/P ratios did not differ significantly between tumorous and normal ribs. X-ray diffraction studies showed that the crystallinity (ie, crystal size/perfection) of the mineral apatite in tumor of the rib from the control horse was lower than that of normal bone from the same rib. Fluoride, however, induced a marked change in the crystallinity at both the tumorous and the normal bone sites. The crystallinity of the tumor apatite in the fluoride-fed horse exceeded that of normal bone in the control horse. Otherwise, there were not demonstrable fluoride-induced gross or radiographic changes in the bone tumors.

Animals↗

Nicotiana glauca-induced congenital deformities in calves: clinical and pathologic aspects.

Seven calves born to 7 cows fed Nicotiana glauca during portions of the 1st trimester of gestation were deformed at birth. Deformities increased in severity as the calves aged. At birth, calves typically had arthrogryposis of the forelimbs or curvature of the spine; severity varied among calves. In 4 calves necropsied at about 15 months of age, there was general malpositioning and misalignment of the distal ends of the radius and ulna and the proximal ends of the metacarpal bones. Carpal joints were severely affected, fetlock joints were moderately affected, and pastern joints were slightly affected, with lateral rotation of forelimbs common; severity varied among calves. In 1 of the 4 calves, there was moderate torticollis and scoliosis resulting from wedging of some of the cervical and thoracic vertebrae and abnormal cranial curvature of the left thoracic ribs. Histologic changes were not noticed in muscle, brain, spinal cord, or endocrine organs of the 4 calves.

Abnormalities, Multiple↗

Clinicopathologic features of fluoride toxicosis in cattle.

Cattle normally ingest variable low-level amounts of fluorides with no known adverse effects, but when excessive amounts are ingested, adverse effects are induced. Several sources may contribute to the total fluoride intake. The many recognized factors that influence structural and functional responses of animals to fluorides are cited. Signs and lesions of fluoride toxicosis in cattle have been characterized. Major fluorotic lesions occur in the permanent teeth and in the bones. Dental lesions occur when excessive amounts of fluoride are ingested during the period of tooth formation and calcification. Bone effects can be induced at any time during an animal's life. A table relating structural changes and functional processes in cattle of various ages has been compiled as a guide for diagnosing and evaluating fluoride toxicosis. Recommended fluoride tolerance levels for cattle have been established. Prevention and control of fluoride toxicosis in cattle can be accomplished when the nature of the disease is realized; the symptomatology, lesions and pathogenesis are properly interpreted, correlated and evaluated; and the source(s) of excessive fluorides are eliminated.

Animals↗

Teratogenicity and toxicity of coniine in cows, ewes, and mares.

Cows, ewes, and mares varied considerably in susceptibility to toxicoses from the oral administration of the piperidine alkaloid, coniine. Cows were most susceptible and ewes least. Only calves had teratogenic effects from maternal administration of coniine during gestation; lambs and foals were apparently resistant. Results suggest that the marked differences between cattle and sheep are probably not due to variation in gut absorption or rumen metabolism.

Abnormalities, Drug-Induced↗