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Biomedical subjects

B G Boysen

Publications and source records attributed to B G Boysen.

17 recordsLinked to original sources
PubMed1998

Oral toxicity and carcinogenicity studies of sucrose acetate isobutyrate (SAIB) in the Fischer 344 rat and B6C3F1 mouse.

Sucrose acetate isobutyrate (SAIB), a food additive used as a flavour emulsion stabilizer in citrus-based soft drinks, was evaluated for chronic toxicity in B6C3F1 mice and Fischer 344 rats. SAIB dissolved in acetone was blended into NIH07 rodent diet at concentrations that were adjusted weekly during the first 12 to 18 months of the studies so that ingested dose levels per kg body weight were constant. Groups of 20 rats per sex were given dose levels of 0.0, 0.0, 0.5, 1.0 and 2.0 g SAIB/kg body weight for 1 yr, and groups of 50 rats per sex were given dose levels of 0.0, 0.0, 0.5, 1.0 and 2.0 g SAIB/kg body weight for 2 yr. Mice were fed dose levels of 0.0, 0.0, 1.25, 2.5 and 5.0 g SAIB/kg body weight for 2 yr. The highest doses fed, equivalent to dietary concentrations of approximately 5%, were considered to be the maximum concentrations that could be fed without risk of nutritional deficiencies. Depressions in body weight gain were noted, particularly in female rats during the first 12 to 18 months of the studies. Recovery during the last quarter of the 2-yr study suggests that the reduced body weight gain was nutritional rather than SAIB-related. There were no differences in survival between SAIB-treated rats or mice and controls. Decreased body weight gains, primarily in females, but less consistent than those in the rat, were noted in the 2-yr mouse study. No signs of toxicity were observed in clinical chemistry, haematology, organ weights, gross necropsy findings or light microscopy studies in the 1- or 2-yr rat studies. Electron microscopic examinations of liver sections from high dose level rats from the 1-yr study also revealed no effects of SAIB treatment. There were no significant increases in benign or malignant tumours in the long-term rat or mouse carcinogenicity studies. The lowest no-observed-adverse-effect level (NOAEL) was 2 g SAIB/kg body weight derived from the 1- and 2-yr chronic toxicity studies in the rat.

Animal Feed↗
PubMed1998

Sucrose acetate isobutyrate (SAIB): three-generation reproduction study in the rat and teratology studies in the rat and rabbit.

A three-generation reproduction study of sucrose acetate isobutyrate (SAIB) in Fischer 344 rats and teratology studies in Fischer 344 rats and New Zealand white rabbits were performed. Dietary SAIB concentrations to provide dose levels of 0, 0.5, 1.0 and 2.0 g/kg body weight were used for the rat studies, and 0, 0.5, 0.85 and 1.2 g/kg body weight doses of SAIB in corn oil were administered by gavage in the rabbit studies. F0 generation male rats were fed SAIB for 10 wk, and female rats were fed SAIB for 2 wk prior to mating. F1 generation rats were raised on the test diets to maturity, mated to produce F2a litters, and remated to produce the F2b litters that were examined for teratology. F2a rats were mated to study fertility indices for the F3 pregnancy. A decrease in female fertility compared with controls was noted at the highest dose of SAIB during breeding of the F1 generation to produce the F2a litters. No difference in fertility rate between controls and treated animals was noted in the results of the other three matings that were performed, and it was concluded that the reduction in female fertility was not related to SAIB treatment. No morphological abnormalities of soft tissue or skeleton were observed in the rat or rabbit teratology studies. The highest dose levels administered, 2.0 g SAIB/kg body weight in the rat and 1.2 g SAIB/kg body weight in the rabbit, were considered to be no-observed-adverse effect levels (NOAEL).

Animal Feed↗
PubMed1993

Confounded carcinogenicity study of sodium fluoride in CD-1 mice.

To determine its carcinogenic potential, sodium fluoride (NaF) was fed to CD-1 mice for up to 97 weeks. Mice given NaF at a dose of 4, 10, or 25 mg/kg of body weight per day added to a low-fluoride diet were compared to controls given either an unsupplemented low-fluoride diet or laboratory chow. Nonneoplastic changes consistent with those previously recognized from fluoride toxicity were observed in teeth, bones, and joints. Unexpectedly, osteomas occurred in all groups. The incidence of osteomas was similar in groups given the low-fluoride control diet, laboratory chow, or NaF doses of 4 or 10 mg/kg per day. The incidence of osteomas in these groups was increased over that historically experienced at the laboratory and reported in the literature for CD-1 mice. The incidence of osteomas in the mice given 25 mg NaF/kg per day added to a low-fluoride diet was increased over that in the other groups. Osteomas were first observed at Week 55. No malignant bone tumors were observed during the course of the study. The locations, multiplicity, and morphologic features of the osteomas in all groups were similar to those associated with virus-induced bone tumors. Electron microscopic examination revealed abundant retrovirus particles in all osteomas examined from control and test mice. It was concluded that the study was confounded by a retrovirus which contributed to the induction of the osteomas. Because the study was confounded, it cannot be considered a valid bioassay to be used for risk assessment.

Animals↗
PubMed1992

Toxicity studies of Caramel Colour III and 2-acetyl-4(5)-tetrahydroxybutylimidazole in F344 rats.

Caramel Colour III is used as a colour additive in beers and a variety of foods. Beer is the most important single source of Caramel Colour III in the diet although consumption of dark beers has been decreasing in recent years. The Joint FAO/WHO Expert Committee on Food Additives (JECFA) has established an acceptable daily intake of 200 mg/kg/day for Caramel Colour III. The safety of Caramel Colour III has been questioned during recent years following feeding studies in the rat that were associated with reduced white cell and lymphocyte counts. These effects have been attributed to the presence of 2-acetyl-4(5)-tetrahydroxybutylimidazole (THI) in this class of caramel colour. Short-term oral toxicity studies were conducted on low-THI and high-THI samples of Caramel Colour III (13 wk) and on a sample of THI (28 days). In both studies, the test materials were mixed with demineralized water and the solutions were given to the animals ad lib. in the drinking fluid. In the 13-wk subchronic toxicity study of Caramel Colour III, groups of 20 rats/sex were given concentrations of caramel colour equivalent to intakes of 0, 10, 15 or 20 g low-THI caramel colour/kg body weight/day or 20 g/kg of a high-THI caramel colour. In the 4-wk toxicity study with THI, groups of 20 rats/sex were given 0, 8 or 64 ppm THI (equivalent to approx. 0, 0.9 or 7.2 mg/kg/day) and 10 rats/sex were given 1, 2, 4, 16 or 32 ppm THI (equivalent to approx. 0.1, 0.2, 0.5, 1.9 or 3.7 mg/kg/day) for 4 wk followed by a 2-wk recovery phase for 10 rats/sex in the 0, 8 and 64 ppm groups. Rats given Caramel Colour III had soft faeces; there were no other treatment-related clinical observations and no treatment-related deaths occurred. All treated groups given Caramel Colour III had lower food and fluid consumption than controls. Males given 15 or 20 g low-THI caramel colour/kg or 20 g high-THI caramel colour/kg and females given 20 g/kg of either type had lower body weights than controls. In the 4-wk toxicity study with THI, there were no treatment-related ante-mortem observations, and no effects on body weights or food consumption. Fluid consumption by males and females treated with 64 ppm THI was lower than that of controls.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Oral↗
PubMed1992

Toxicity and carcinogenicity studies of Caramel Colour IV in F344 rats and B6C3F1 mice.

Caramel Colour IV, a type of caramel colour used in the manufacture of cola soft drinks, was evaluated for subchronic and chronic toxicity in rats, and carcinogenicity in Fischer-344 (F344) rats and B6C3F1 mice. In each of the studies, Caramel Colour IV was mixed with demineralized water and the solutions given to the animals ad lib. in the drinking fluid. The concentrations of Caramel Colour IV in the drinking fluid were adjusted periodically to achieve the desired caramel colour intake per kg body weight. In the range-finding studies, groups of 30 rats/sex were given Caramel Colour IV at levels of 0, 15, 20, 25 or 30 g/kg for 13 wk, and groups of 10 male rats were given levels of 0, 2.5, 5, 10 or 15 g/kg for 6 wk followed, for some dose groups, by a 2-wk withdrawal period, and then re-initiation of dosing for another 2 wk. In the rat chronic toxicity study, levels of Caramel Colour IV of 0, 2.5, 5, 7.5 or 10 g/kg were given to groups of 25 rats/sex for 12 months. The test groups in the rat and mouse carcinogenicity studies were composed of 50 animals/sex and each species was given the caramel colour at levels of 0, 0, 2.5, 5 or 10 g/kg for 24 months. In each of the studies, treated animals tended to have dose-related lower water consumption than controls. This was attributed to poor palatability of the drinking fluid, and was generally associated with decreased food consumption and body weights. Rats given caramel colour often had soft or liquid malodorous faeces although there were no treatment-related ante-mortem observations in mice. Blood biochemical changes in the rat (i.e. reduced blood urea nitrogen, alkaline phosphatase and total serum protein) appeared to be related to dietary influences and were not considered toxicologically significant. There were no treatment-related alterations in haematological variables or treatment-related differences in survival or in the incidence of benign or malignant tumours among treated and control groups and no toxicologically important pathological findings. On the basis of these studies, Caramel Colour IV was not toxic or carcinogenic in F344 rats or B6C3F1 mice. The highest dose level tested in the long-term studies (10 g/kg) was considered to be the no-observed-adverse-effect level (NOAEL).

Administration, Oral↗
PubMed1992

Response of dairy cows to high doses of a sustained-release bovine somatotropin administered during two lactations. 2. Health and reproduction.

Eighty-two lactating Holstein cows in their first, second, or third lactation received either one, three, or five concurrent i.m. injections of a unit dose (.6 g) of zinc methionyl bST (sometribove) or five doses of the vehicle. Injections were given at 14-d intervals from 60 +/- 3 d postpartum until the end of lactation or necropsy. Thirty-eight animals were continued on treatment for a 2nd yr. Sometribove did not affect the incidence of ketosis, milk fever, tetany, or pneumonia. Digestive disorders, primarily cows going off feed, were increased by bST during yr 1 only. The incidence of lameness was increased by bST in some time frames because of an increase in the 3.0-g bST group. Lameness was not associated with treatment-specific histopathologic changes or with abnormalities in cartilage or bone. Reproductive health generally was unaffected by treatment, but delayed conception and increased incidence of abortion were noted. Incidence of cystic ovaries was unaffected by bST. Pregnancy rates were decreased during the 100-d breeding interval of yr 1 but not during the 215-d interval of yr 2. The incidence of clinical mastitis was increased by bST, primarily at the 3.0-g dose. During the 2-yr study, 0, 3, 3, and 2 cows died or became moribund on 0, .6, 1.8, and 3.0 g of bST, respectively. Health issues identified for further evaluation included lameness and clinical mastitis for the 3.0-g group and early removal from the herd and decreased reproductive performance for all bST groups. Bovine somatotropin caused no treatment-specific toxic effects in dairy cows even at 3.0 g every 14 d.

Animals↗
PubMed1992

Effect of high doses of a sustained-release bovine somatotropin on antibody formation in dairy cows.

Eighty-two lactating Holstein cows received either one, three, or five concurrent, intramuscular injections of a unit dose (.6 g) of zinc methionyl bST (some-tribove) or five doses of the vehicle. Injections were administered at 14-d intervals from 60 d postpartum until the end of lactation or necropsy. Thirty-eight cows continued on the same treatment for a 2nd yr. Blood bST antibodies developed within the first 7 wk of treatment, and the number of cows with anti-bST binding generally declined with time. Thirteen out of 59 cows receiving bST developed binding activity > 25% (positives) during the 1st yr. At the .6-g dose level, no binding was detected after wk 15. Seven of the 13 positive cows were among the group randomly selected to continue on study during yr 2. In the 2nd yr, only 2 out of 24 bST-treated cows were positive. Binding activity was associated with the IgG fraction in serum. Binding capacities of antibodies ranged from .625 to 3.04 mg of bST/L, and affinities ranged from 1.14 x 10(8) to 3.14 x 10(8) L/mol. Cows considered to be clinically positive had performance similar to those of their herdmates having binding < 25%. No evidence of a pathologic effect of antibodies existed in treated cows, their calves, or fetuses. The presence of anti-bST antibodies did not affect milk production of the cow or growth of the calves conceived during bST treatment.

Animals↗
PubMed1991

A neurotoxicity screening battery for use in safety evaluation: effects of acrylamide and 3',3'-iminodipropionitrile.

The effects of two known neurotoxicants, acrylamide (ACR) and 3',3'-iminodipropionitrile (IDPN), were assessed using a functional observational battery (FOB), a measurement of motor activity (MA), and neuropathology (NP) in the context of a safety evaluation study. One hundred Sprague-Dawley rats (10/sex/group) were tested initially and then doses with vehicle, ACR (10 or 30 mg/kg/day), or IDPN (50 or 125 mg/kg/day) by oral gavage 7 days/week for 5 weeks (except where otherwise indicated). Neurobehavioral assessments were conducted prior to initiating treatment at 1, 6, and 24 hr after the first dose, and weekly thereafter. Body weight and food consumption were determined weekly, and animals were observed twice daily for signs of toxicity. Blood samples were obtained at termination for routine clinical pathology studies. At termination three animals/sex/group were perfused in situ for neuropathology evaluations and the remaining animals were necropsied for standard histological evaluations. Prominent neurological signs were observed in high-dose animals after 2 weeks, and significant mortality occurred in high-dose ACR animals during Week 3. A 7- or 10-day recovery period was initiated after 20 or 22 daily doses for high-dose IDPN and ACR animals, respectively. ACR and IDPN affected body weight, body-weight gain, food consumption, general activity (horizontal and vertical), urination, muscle tone (grip strength), motor reflexes, gait, and posture. Significant sex effects were seen in animals exposed to IDPN, with males being more severely affected. Microscopic examination of nervous system tissue and selected organs revealed minimal to moderately severe axonal swelling characterized by the presence of enlarged balloon-like axons in the brainstem and the cervical and lumbar cord of IDPN-treated animals. This change was most prominent in males and most severe in the lumbar spinal cord. An increased incidence of chronic progressive nephropathy was also noted in IDPN-treated rats. ACR-treated animals exhibited minimal to moderate degeneration in the cervical and lumbar spinal cord, the gasserian and dorsal root ganglia, and the tibial, sciatic, and sural nerves which were characterized by changes in axonal diameter, increased argyrophilia of axons, and disruption, fragmentation, and distortion of axons and the myelin sheath. Granulomatous inflammation in the lungs of high-dose ACR animals resulted from inhalation of feed, most probably due to partial paralysis or incoordination during feeding.

Acrylamide↗
PubMed1990

Two-year carcinogenicity study of sodium fluoride in rats.

To determine the carcinogenic potential of sodium fluoride (NaF), we fed Sprague-Dawley rats a diet containing NaF for up to 99 weeks. Rats receiving NaF at a dose of 4, 10, or 25 mg/kg per day added to a low-fluoride diet were compared with controls receiving either a low-fluoride diet or laboratory chow. Each treatment group consisted of 70 rats of each sex. A 30% decrement in weight gain occurred at an NaF dose of 25 mg/kg per day. Evidence of fluoride toxicity was seen in the teeth, bones, and stomach, and the incidence and severity of these changes were related to the dose of NaF and the duration of exposure. Despite clear evidence of toxicity, NaF did not alter the incidence of preneoplastic and neoplastic lesions at any site in rats of either sex. Results from this study indicate that NaF is not carcinogenic in Sprague-Dawley rats.

Animals↗
PubMed1987

Temporal analysis of dithiobiuret neurotoxicity in rats and assessment of potential nonneural causes.

To evaluate the hypothesis that depressed neuromuscular transmission causes dithiobiuret (DTB)-induced muscle weakness in rats, the temporal development of impaired treadmill performance and deficits in the nerve-elicited muscle contractions were compared during daily treatment with the toxicant (DTB, 1 mg/kg/day X 6 days). Diminished treadmill test performance after 4 days of treatment marked the initial detection of impaired motor function. At this time fading (loss of tension during tetanus) of gastrocnemius contractions elicited in response to 100-Hz sciatic nerve stimulation occurred in DTB-treated rats but not in controls. After 5 and 6 days of treatment, treadmill failure became complete, tetanic fade worsened dramatically, and peak contractile tension measured during trains of nerve stimulation (10-250 Hz) decreased progressively. Appearing by Day 6 were marked body weight loss, dehydration, hypothermia, and a depression in serum concentrations of thyroid hormones. Total oxygen content of the blood was not reduced at any time during treatment, and serum concentrations of glucose, sodium, potassium, calcium, chloride, and phosphorus in DTB-treated rats on Day 6 were similar to those of control animals. Therefore, hypoxia, hypoglycemia, or a serum electrolyte imbalance do not initiate or modulate the neuromuscular toxicity. Light microscopic evaluation of liver, kidney, lung, thyroid, and other organs in intoxicated rats was unremarkable and in skeletal muscles and selected sites of brain, spinal cord, and sciatic nerve no morphologically significant lesions were observed. Even when DTB-intoxicated rats were maintained in a state of flaccid muscle weakness for 5 continuous days, peripheral nerve lesions proximal to the intramuscular nerves were not detected. Thus, depressed neuromuscular transmission appears to be the primary cause of the flaccid muscle weakness and no evidence was obtained that nonneural effects of DTB initiate or modulate this effect.

Animals↗
PubMed1978

Acute necrotizing myelopathy from nucleus pulposus embolism in dogs with intervertebral disk degeneration.

Two dogs that suddenly developed neurologic signs indicating a severe cervical spinal cord lesion were found at necropsy to have necrotizing myelopathy secondary to nucleus pulposus embolism. One dog had embolism of arteries and veins; in the other dog, veins alone were embolized. Each dog had early degeneration and extrusion of the C6--7 disk, from which emboli originated. In one dog, arterial emboli apparently entered inflammatory vasculature in the anulus fibrosus and were forced by extrusion back through the arterial system to the radicular artery and then to the cord. Venous embolism occurred secondarily to arterial embolism. In the other dog, venous embolism resulted from direct herniation of nucleus pulposus into the longitudinal venous sinus. A comparison of the pathogenesis of embolization in each case and a survey of other reported cases suggested that necrotizing myelopathy is a complication of early degeneration of intervertebral disks in large dogs.

Animals↗
PubMed1978

Listeriosis in an Arabian foal with combined immunodeficiency.

A 1-month-old Arabian foal with signs of central nervous system disease was found to have combined (B- and T-lymphocyte) immunodeficiency. The foal died in spite of intensive antibiotic therapy. At necropsy, generalized lymphoid hypoplasia and acute necrotizing and granulomatous inflammation of the brain, heart, and adrenal glands were found. In addition, there were spinal meningitis and focal hepatic necrosis. Listeria monocytogenes was isolated on primary culture from the brain.

Animals↗
PubMed1976

Myopathy and myoglobinuria in a wild white-tailed deer.

Fatal myopathy similar to "capture myopathy" described for African game was diagnosed in a wild white-tailed deer. Clinical signs included depression, inability to rise or stand, and myoglobinuria. Values for serum creatine phosphokinase, glutamic oxaloacetic transaminase, and blood urea nitrogen were high. The deer died 42 hours after capture. At necropsy the muscles of the limbs had a waxy, "cooked" appearance and the kidneys were brown. Microscopic findings included severe degeneration and fragmentation of skeletal muscle fibers, nephrosis, centrilobular hepatic necrosis, myocardial degeneration, and anoxic neuronal degeneration.

Animals↗