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Biomedical subjects

W M Haschek

Publications and source records attributed to W M Haschek.

89 records · Page 5Linked to original sources
PubMed1979

The influence of hyperoxia on the acute toxicity of paraquat and diquat.

Hyperoxia has been shown to enhance the toxicity of the herbicide paraquat. Experiments were conducted to learn more about the effects of oxygen following acute poisoning with paraquat as well as the structurally related herbicide, diquat. Rats were injected intravenously with various doses of diquat or paraquat and placed into an atmosphere of either 100% oxygen or room air. The time required for 50% lethality (LT50) of both diquat and paraquat was greatly diminished by hyperoxia and was dependent upon the herbicide dosage. Rats treated with 40 or 80 mg/kg diquat and exposed to 100% oxygen had a shorter LT50 than those treated similarly with paraquat. A dose of 20 mg/kg was equitoxic in 100% oxygen while rats treated with 5 or 10 mg/kg diquat had a longer LT50 than rats treated with the same dose of paraquat. All animals exhibited severe respiratory distress terminally. The plasma concentrations and tissue distribution of either herbicide at 20 mg/kg were the same in oxygen and air exposed animals. When oxygen concentrations were varied between 100% and 60% rats treated with 20 mg/kg diquat or paraquat exhibited increasing but equal LT50's. In 40% oxygen diquat treated rats died more rapidly than paraquat treated rats. These data demonstrate a toxic interaction between hyperoxia and diquat as well as paraquat.

Animals↗
PubMed1979

Element and polychlorinated biphenyl deposition and effects in sheep fed cabbage grown on municipal sewage sludge.

Sheep were fed a diet containing 30 per cent (dry weight) cabbage which had been grown on municipal sewage sludge from Syracuse, NY for 77 days. Slight increases were found in the concnetration of nickel in kidney, copper in liver and cadmium in certain animal organs as compared to those in sheep fed a control ration containing cabbage grown on soil. Polychlorinated biphenyls were also found at higher levels in the sludge-grown cabbage and in the livers of the respectively fed sheep as compared to controls. An increase in liver weight, proliferation of hepatic smooth endoplasmic reticulum and various degenerative changes were noted in the livers of the sheep fed the sludge-grown cabbage ration as compared to the controls.

Animal Feed↗
PubMed1979

Toxicologic studies with sheep fed colored magazines and newsprint.

Paper containing colored inks from magazines and newspapers was fed as 23% of their ration to sheep for 175 days. A similar ration containing oat hulls in place of the paper was fed to control animals. The paper-fed animals consumed 29% more feed than the controls but the feed efficiency (kg animal weight gained/kg ration consumed) of the two rations was approximately equivalent. Lead contained in the paper accumulated in animal tissues. Hepatic microsomal mixed function oxidase activity was several fold higher in the paper-fed animals than the controls. Histopathologic examination of liver and kidney using light and electron microscopy revealed no lesions attributable to diet.

Animal Feed↗
PubMed1979

Ostertagiosis in captive bison in New York State: report of nine cases.

Type II ostertagiosis was found at necropsy in 9 American bison (Bison bison) from 3 farms in New York. Clinical signs included severe diarrhea, emaciation, unthrifty coats, anemia, and weakness. In severely affected animals, the macroscopic abomasal changes consisted of irregular thickening and edema of the mucosa, resulting in a pebbly or morocco-leather appearance. Microscopically, many gastric pits and glands were dilated, lined by hyperplastic epithelium, and contained nematode sections or debris. Parasites recovered included Ostertagia ostertagi, Trichostrongylus axei, Trichostrongylus lerouxi, Cooperia oncophora, Haemonchus contortus, Nematodirus helvetianus, Trichuris discolor, Setaria labiato-papillosa, Dictyocaulus viviparus, Hypoderma lineatum, and Sarcocystis sp. Nodules in the small and large intestine were attributed to Oesophagostomum sp. Trichostrongylus lerouxi, Trichuris discolor, and Nematodirus helvetianus are reported from bison for the first time.

Abomasum↗
PubMed1978

Vitamin D toxicity. Initial site and mode of action.

Two groups of weanling pigs, injected with 45Ca, were fed diets containing optimal calcium and phosphorus, and vitamin D3 at 1320 IU/kg feed in the control group, and 825,000 IU/kg feed in the test group. The groups were further subdivided with 2 pigs in each subgroup, with survival times of 1, 2, 3, 4, 7, and 14 days. Pigs fed the high level of vitamin D3 lost weight and anorexia, weakness, rough hair coat and labored breathing were observed. Hypercalcemia began at 12 hours and progressed rapidly after 2 days. Radioisotope sutdies interpreted in the light of histopathologic findings indicated that bone was the primary source of increased plasma calcium. Calcium was released at a rapid rate into blood from prelabeled bone which was undergoing necrosis; it was also removed from blood and deposited into bone at a slower rate due to decreased apposition. Histopathologic examination of bones from test pigs showed regressive changes in the osteocytes, chondrocytes and osteoblasts which bean within 1 day of treatment and resulted in evidence osteopenia within 7 days. Arrested osteocytic osteolysis led to the appearance of cementing lines and to chondroid core retention. Further regressive changes in the osteocytes resulted in osteocytic death and osteonecrosis with subsequent osteoclasia and osteopenia. Retardation and arrest of cartilage maturation as well as osteoblastic deficiency contributed to the osteopenia. The osteopenia was further evidenced by decreased specific gravity and ash content per unit volume of humerus. The initial negative effect on the osteocytes, chondrocytes and osteoblasts is attributed to a direct toxic effect of excessive dietary vitamin D3 since hypoparathyroidism and hypercalcitoninism, which occur secondarily to hypercalcemia, could not account for the rapid appearance of this effect, nor are they known to induce osteocytic death. The release of bone calcium and the resulting hypercalcemia in vitamin D3 toxicosis is therefore due to a direct toxic effect of the vitamin, or its metabolites, on the osteocyte resulting in osteonecrosis. It is not due to increased resorption as has been reported previously from both in vivo and in vitro investigations. Degeneration, with subsequent inflammation, but without calcification, was observed in the kidneys and in the lungs. Epithelial cells, basement membranes, and smooth muscle were affected. This conclusively demonstrates that degeneration is the primary soft tissue lesion in vitamin D3 toxicosis, and that the subsequent calcification is therefore dystrophic. Degenerative changes occurred in the parathyroid glands within 1 day of treatment resulting in necrosis, inflammation and atrophy within 4 days. Relative fibrosis was seen as the parenchyma receded. The parathyroid gland changes were considered a direct effect of vitamin D3 toxicity since they occurred with only mild hypercalcemia and since necrosis of parathyroid cells has not been demonstrated with hypercalcemia either in vivo or in vitro.

Animals↗
PubMed1977

Diaphragmatic hernias in the horse: a review of the literature and an analysis of six additional cases.

Eighteen cases of equine diaphragmatic hernia were reviewed. Most of the cases were of long duration, with an additional factor precipitating acute abdominal crisis. History and physical examination were of little diagnostic significance. Radiography, if available, and exploratory laparotomy were the most useful diagnostic procedures. The prognosis for successful surgical repair and recovery was poor.

Animals↗
PubMed1977

Selenium and white muscle disease in woodchucks.

Gross and histologic examination of wood chcks (Marmota monax) trapped on farms in Central New York revealed white muscle disease(WMD). The concentration of selenium in the animal tissues, vegetation and soils in the vicinity of trapping did not consistently correlate with the presence of WMD.

Animals↗
PubMedDate not supplied

Heavy metal residues in plants cultivated on and in small mammals indigenous to old orchard soils.

Six vegetables and millet were grown on the site of an old orchard which had received heavy applications of lead arsenate and organic mercury fungicides for many years. Carrots and millet absorbed about 7 ppm (dry weight) of lead, the other crops containing smaller concentrations. Concentrations of arsenic and mercury showed only modest increases in crops grown on the orchard soil as compared to controls. Lead concentrations in kidney, liver, and bone tissue of meadow voles trapped in two old orchards were markedly higher (up to 300 ppm in bone) than control animals (up to 33 ppm). Intranuclear inclusion bodies diagnostic of lead poisoning were found in the renal epithelial cells of the proximal convoluted tubules in voles from lead arsenate treated orchards.

Animals↗
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

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↗