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Biomedical subjects

V R Beasley

Publications and source records attributed to V R Beasley.

88 records · Page 5Linked to original sources
PubMed1985

Experimental T-2 toxicosis in swine. I. Changes in cardiac output, aortic mean pressure, catecholamines, 6-keto-PGF1 alpha, thromboxane B2, and acid-base parameters.

T-2 toxin given as a single intravascular dose to swine produced a shock syndrome. Dosages of 0.6 or 4.8 mg/kg were administered to different groups of swine. Shock was characterized by reductions in cardiac output and blood pressure, and increased plasma concentrations of epinephrine, norepinephrine, thromboxane B2, 6-keto PGF1 alpha, and lactate. Total peripheral resistance was unchanged in the high-dose group but decreased in the low-dose group. Pulmonary vascular resistance increased in both groups. Decreases occurred in arterial pH and arterial oxygen partial pressure. No alterations occurred in plasma concentrations of histamine or serotonin.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Experimental T-2 toxicosis in swine. II. Effect of intravascular T-2 toxin on serum enzymes and biochemistry, blood coagulation, and hematology.

T-2 toxin was given as a single intravascular dose at either 0.6 or 4.8 mg/kg to different groups of 50-kg female swine. Blood samples were taken at hourly intervals for determination of concentrations or activities of the following substances in serum or plasma: creatinine, blood urea nitrogen, inorganic phosphorus, total calcium, ultrafilterable calcium, magnesium, sodium, potassium, chloride, total protein, albumin, cholesterol, glucose, alkaline phosphatase, aspartate aminotransferase, and total bilirubin. Coagulation analyses included prothrombin time, partial thromboplastin time, activated coagulation time, and fibrin degradation products. Red blood cell, white blood cell, and platelet counts, hemoglobin concentrations, and hematocrits were determined from whole blood samples. An initial leukocytosis was followed by a leukopenia. The numbers of red cells, the hemoglobin concentration, and the hematocrit were increased. Nucleated red blood cells were seen in the blood smears. The serum concentration of bound calcium decreased, while phosphorus, magnesium, and potassium increased. Clinical screening tests detected no evidence of a coagulopathy in swine given T-2 toxin intravascularly.

Alkaline Phosphatase↗
PubMed1985

Sex-related reduced weight gains in growing swine fed diets containing deoxynivalenol.

A 5-wk feeding trial was conducted with 30 castrated male and 28 female, 5-wk-old crossbred piglets. Three different deoxynivalenol (DON) and zearalenone (Z)-contaminated diets were fed: .7, 3.1 and 5.8 ppm DON and 0, .05, and .1 ppm Z, respectively. The animals were fed their respective diets for 4 wk followed by the .7:0-ppm diet during wk 5. Feed intake and weight gain varied in a manner reciprocal to the levels of DON-Z in the diets during the first 4 wk (P less than .05). The castrated males had an overall lower weight gain compared with the females receiving the same diet (P less than .05). Gross postmortem changes were not different in either sex and tended to be most prominent in the pigs fed the lower DON:Z-contaminated diets after the first week, although they were seen in pigs fed the higher DON:Z diets after 4 wk of feeding. Lesions included mild to moderated reddening of the fundic mucosa of the stomach, reddening of the mucosa of the small intestine, and mild to moderate enlargement and edema of the mesenteric lymph nodes. Similarly, the severity of histologic changes tended to vary inversely with the concentrations of DON:Z in the diets after the first week but varied with the concentrations of DON:Z after 4 wk. They consisted of vascular congestion with mild to moderate multifocal erosions and degeneration of the mucosa in the stomach and small intestine. Mild to moderate lymphoid degeneration and depletion were also observed in the Peyer's patches of the intestines, bronchial and mesenteric lymph nodes, spleen, tonsil and thymus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1984

Industrial lead contamination of an Illinois wildlife refuge and indigenous small mammals.

Deer mice (Peromyscus maniculatus) were trapped from a sand prairie at various distances from an adjacent battery lead reclamation plant. Analysis of liver, kidney, and bone for lead concentrations showed an increase of tissue lead concentrations over controls to a distance of approximately 400 m. Soil and plant lead concentrations roughly correlated with the findings in deer mouse tissues. At higher tissue lead concentrations, acid-fast staining intranuclear inclusions within renal tubular epithelial cells were an occasional finding.

Animals↗
PubMed1983

Gas-liquid chromatographic determination of T-2 toxin in plasma.

A gas-liquid chromatographic method for the determination of T-2 toxin in plasma is described. The toxin is extracted with benzene, washed with aqueous sodium hydroxide, and chromatographed on a small Florisil column; the heptafluorobutyryl derivative is prepared by reaction with heptafluorobutyrylimidazole. The T-2 HFB derivative is chromatographed on OV-1 at 230 degrees C and measured with an electron capture detector. Iso-T-2, an isomer of T-2 toxin, is added to samples as an internal standard before extraction. Recoveries averaged 98.0 +/- 5.5% at levels ranging from 50 to 1000 ng/mL. The limit of detection is 25 ng/mL.

Chromatography, Gas↗
PubMedDate not supplied

A wire reclamation incinerator as a source of environmental contamination with tetrachlorodibenzo-p-dioxins and tetrachlorodibenzofurans.

The authors investigated an outbreaks of unusual illnesses in humans and horses residing within 1.3 km of a wire reclamation incinerator. The study included site visits; medical and veterinary examinations; analyses of furnace ash, fly ash, soil, and biologic samples for air residues. Tetrachlorodibenzo-p-dioxins (TCDDs) and tetrachlorodibenzofurans (TCDFs) were discovered in furnace ash, fly ash, soil, horse fat, and horse liver samples.

Adult↗
PubMedDate not supplied

Alterations in microtubules, intermediate filaments, and microfilaments induced by microcystin-LR in cultured cells.

Microcystin-LR (MCLR) is a cyanobacterial hepatotoxin that inhibits intracellular serine/threonine protein phosphatases causing disruption of actin microfilaments (MFs) and intermediate filaments (IFs) in hepatocytes. This study compared the effects of MCLR on the organization of MFs, IFs, and microtubules (MTs) in hepatocytes and nonhepatocyte cell lines and determined the sequence of toxin-induced changes in these cytoskeletal components. Rat renal epithelial cells and fibroblasts were incubated with MCLR at 100 or 200 microM for 6-18 hr. Rat hepatocytes in primary culture were exposed to the toxin at 1 or 10 microM for 2-64 min. Cells were fixed and incubated with primary antibodies against beta-tubulin, actin, and vimentin or cytokeratin IFs, followed by gold-labeled secondary antibodies with silver enhancement of the gold probe. The fraction of fibroblasts and hepatocytes with altered cytoskeletal morphology was evaluated as a function of MCLR dose and exposure time to assess the sequence of changes in cytoskeletal components. Changes in fibroblasts and some hepatocytes were characterized initially by disorganization of IFs, followed rapidly by disorganization of MTs, with the progressive collapse of both cytoskeletal components around cell nuclei. Many hepatocytes exhibited MT changes prior to effects on IF structure. Alterations in MFs occurred later and included initial aggregation of actin under the plasma membrane, followed by condensation into rosette-like structures and eventual complete collapse into a dense perinuclear bundle. The similarity of effects among different cell types suggests a common mechanism of action, but the independent kinetics of IF and MT disruption in hepatocytes suggests that there may be at least 2 sites of phosphorylation that lead to cytoskeletal alterations.

Actin Cytoskeleton↗
PubMedDate not supplied

Rhamnus cathartica (buckthorn) hepatocellular toxicity in mice.

The toxicity of the plant Rhamnus cathartica was assessed in mice after the plant was identified as a potential cause of an idiopathic neurologic disease in horses. Another member of the Rhamnaceae family, Karwinskia humboldtiana, is neurotoxic to mammals and birds and can induce hepatic degeneration and necrosis. To investigate the toxicity of R. cathartica, a 34-day feeding trial in mice was conducted using a complete rodent diet with 0, 5, or 25% added R. cathartica. No clinical signs or gross lesions were seen, and all major tissues were histologically normal except the liver. The livers of mice fed R. cathartica had marked hepatocellular swelling. Results from periodic acid-Schiff reaction staining and from electron microscopy confirmed that the swelling was due to deposits of monoparticulate glycogen (beta particles) in the cytoplasm. Glycogen deposition is an uncommon toxic change in cells. Apparently, compound(s) in R. cathartica directly or indirectly interfered with glycogen metabolism (either glycogenesis or glycogenolysis). Mechanistic and chronicity studies with R. cathartica are needed to investigate the pathophysiology of the glycogen disturbance and to determine if hepatic injury progresses and if other organs will be injured.

Animal Feed↗
PubMedDate not supplied

Development of fumonisin-induced hepatotoxicity and pulmonary edema in orally dosed swine: morphological and biochemical alterations.

The fumonisin (FB) mycotoxins induce liver injury in all species but induce fatal pulmonary edema (PE) only in pigs. They inhibit ceramide synthase in the sphingolipid biosynthetic pathway. To study the pathogenesis of PE, we examined the early events in the development of FB-induced PE and hepatotoxicity in pigs. Pigs were fed FB-contaminated culture material at 20 mg fumonsin B1 (FB1)/kg body weight/day. Groups of 4 pigs were to be euthanatized on 0, 1, 2, 3, 4, or 5 days after initial exposure to FB or when PE developed. Pigs developed PE beginning on day 3; none survived beyond day 4. Progressive elevations in hepatic parameters, including serum enzymes, bile acids, total bilirubin, and histologic changes, began on day 2. Early histologic changes in the lung (day 2) consisted of perivascular edema followed by interlobular and peribronchial edema. Ultrastructurally, alveolar endothelial cells contained unique accumulations of membranous material in the cytocavitary network beginning on day 2. Marked elevations in sphinganine, sphingosine, and their ratio began on day 1 for all tissues whether affected morphologically (lung, liver) or not (kidney, pancreas). The membranous material in endothelial cells may be accumulations of sphingoid bases with damage to the cytocavitary network. Thus, FB induces early elevations in sphingolipids and hepatic injury, followed by alveolar endothelial damage, which may be the critical event in the pathogenesis of PE in pigs.

Animals↗
PubMedDate not supplied

Toxicity of intraperitoneal doses of microcystin-LR in two strains of male mice.

Male Balb/C and Swiss Webster (SW) mice were administered various i.p. doses of microcystin-LR (MCLR) to establish dose-response curves and to determine if a sublethal dose of MCLR would protect against an approximate LD100 min given 2 or 3 days later. Micocystin-LR has an extremely steep dose-lethal response curve in BC mice--LD50 = 32.5 micrograms (micrograms)/kg, approximate LD0 max = 25 micrograms/kg and approximate LD100 min = 40 micrograms/kg. Liver weights increased 64% (BC) and 51% (SW) and kidney weights increased 32% (BC) and 20% (SW) within 200 minutes following administration of an approximate LD100 min of MCLR in naive mice. Grossly and histologically the marked increase in liver weight appeared to be caused primarily from intrahepatic hemorrhage and death is probably a result of hemorrhagic shock. Twenty-four hours following administration of a sublethal dose of MCLR to naive BC mice, liver weights were increased significantly (8.7%), but no clinical signs or histologic lesions were observed. In SW mice, administration of a LD23 of MCLR resulted in significantly increased survivability and survival times when an approximate LD100 min of MCLR was given 3 days later. Survivors of the LD23/LD100 min regimen had 96 hour postdosing liver weights not significantly different from those of mice which died acutely after the same hepatotoxin treatments. These survivors showed weakness, recumbency, anorexia, and icterus, and had marked gross liver lesions. Histologically these lesions were undergoing rapid reparative processes.

Animals↗