Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ducks maintained over winter in an area used for automobile storage and repair were poisoned by anti-freeze. Signs were weakness, depression, ataxia, and death. Post-mortem lesions consisted of marked nephrosis; numerous oxalate crystals occluded the renal tubules. Levels of ethylene glycol were markedly elevated compared with levels in normal tissues. To further characterize the disease, six healthy ducks were given ethylene glycol in oral doses ranging from 1.1 to 17.8 ml/kg. As the dosage was increased, blood and tissue concentrations of ethylene glycol increased and time to death decreased. Histologic lesions were similar to those seen in the accidentally poisoned ducks.
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PMID:Ethylene glycol intoxication in ducks. 702 Jun 83

Signs of acute hemolytic anemia developed in 4 adult horses from 2 Georgia farms 3 to 4 days after the ingestion of wilted leaves from cut red maple trees (Acer rubrum). Clinical findings included weakness, polypnea, tachycardia, depression, icterus, cyanosis, and brownish discoloration of the blood and urine. Blood changes included methemoglobinemia, free plasma hemoglobin, decreased pcv, and Heinz bodies in erythrocytes. These findings plus hemoglobinuria suggested intravascular hemolysis. Three of the 4 horses diet 5 to 7 days after ingestion of the leaves. Gross pathologic changes included generalized icterus, splenomegaly and swollen, black kidneys. Microscopic changes including tubular nephrosis with hemoglobin casts, vacuolization of centrilobular hepatocytes, and sequestration of erythrocytes in splenic sinusoids. A disease indistinguishable from the field cases was induced in a pony by the oral administration of dried, ground red maple leaves at a dosage of 1.5 g/kg. The findings of methemoglobinemia, hemolysis, and Heinz bodies suggested that the toxic principle of the red maple leaf was an oxidant.
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PMID:Hemolytic anemia in horses after the ingestion of red maple leaves. 705 81

Salt poisoning developed in captive sandhill cranes (Grus canadensis) when sea salt was added to normal drinking water to produce a sodium chloride concentration of 1%. Two of 18 cranes died and 2 were euthanatized when moribund. Muscle weakness, paresis, dyspnea, and depression were observed. Brain and serum sodium, serum uric acid, and plasma osmolality values were abnormally high. Lesions were those of visceral gout, renal tubular necrosis, nephrosis, and skeletal muscle necrosis.
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PMID:Iatrogenic salt poisoning in captive sandhill cranes. 732 5

Pregnant CD rats were given vancomycin intravenously in doses of 0, 40, 120, or 200 mg/kg on Gestation Days (GD) 6-15; pregnant New Zealand white rabbits were given 0, 40, 80, or 120 mg/kg intravenously on GD 6-18. Cesarean sections were performed on rats and rabbits on GD 20 and 28, respectively. In rats, maternal toxicity was indicated in the 120- and 200-mg/kg treatment groups by cortical tubular nephrosis. Maternal body weight gain and food consumption and fetal viability, weight, and morphology were not adversely affected by vancomycin. Maternal and developmental no observed adverse effect levels (NOAELs) in the rat were 40 and 200 mg/kg, respectively. In rabbits, maternal toxicity was indicated by cortical tubular nephrosis in the 80- and 120-mg/kg treatment groups; a single death and depression of body weight gain and food consumption occurred in the 120-mg/kg treatment group. Developmental toxicity was indicated by depression of fetal weight in the 120-mg/kg treatment group; fetal viability and morphology were not adversely affected by vancomycin. Maternal and developmental NOAELs in the rabbit were 40 and 80 mg/kg, respectively. Based on these data, vancomycin did not exhibit selective toxicity toward the developing rat or rabbit conceptus.
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PMID:Developmental toxicology studies of vancomycin hydrochloride administered intravenously to rats and rabbits. 786 11

Two sexually intact female silver-shaded domestic ferret siblings from different litters were examined because of CNS depression and lethargy. Ferret 1 was dehydrated and hypothermic, whereas ferret 2 was icteric and febrile and had serum bilirubin concentration > 12.0 mg/dl and BUN of 59 mg/dl. Despite supportive treatment, the ferrets died within days of evaluation. On necropsy, ferret 1 had chronic hepatopathy, with diffuse vacuolation of hepatocytes. In ferret 2, the liver had centrilobular degeneration and necrosis, and hemoglobinuric nephrosis was evident, with hemoglobin in the renal tubules. In both ferrets, Kupffer's cells and macrophages contained eosinophilic material in the cytoplasm. Special staining revealed copper pigment in hepatocytes and phagocytic cells in both livers. Analysis of liver specimens revealed 850 and 700 ppm of copper in ferrets 1 and 2, respectively. Copper values > 200 ppm in liver are considered evidence of toxicosis in most animal species. Copper toxicosis was diagnosed on the basis of the findings from histologic examination of the liver and high hepatic copper values. Lack of related illness in 11 other ferrets in the same environment and fed the same diet, plus sibling relationship and same phenotypic coat color in the affected ferrets, suggested that these ferrets had an inherited defect in their ability to metabolize normal amounts of ingested copper.
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PMID:Copper toxicosis in sibling ferrets. 789 May 74

Three calves received 10 g Riedeliella graciflora dry leaves/kg body weight by gavage. Blood samples were taken immediately before plant administration and at 2, 4, 6, 12 and 24 hours later; serum ALT, AST, AP, TB, urea and creatinine were determined. After R graciflora administration, the calves had anorexia, profound depression and recumbency prior to death. Creatinine levels increased markedly until death. Severe tubular nephrosis was consistently observed.
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PMID:The acute toxicity of Riedeliella graciflora in calves. 859 33

Oncogenicity studies of methyl tertiary-butyl ether (MTBE) vapor were conducted in CD-1 mice and Fischer 344 rats. Fifty animals of each sex per species per group were exposed for 6 h a day, 5 days per week to 0 (control), 400, 3000 and 8000 ppm MTBE vapor in air for 18 months (mice) and 24 months (rats). Both species showed reversible central nervous system depression at 8000 ppm for the first week of exposure, which continued for mice for the study duration. For the 8000 ppm mice, reduced body weight gain and early mortality prior to terminal euthanasia were exposure related. In the males, these deaths appear to be due to exacerbation of uropathy or dysuria, which occurs spontaneously in this strain. Increases in absolute and relative liver (both sexes) and kidney weight (males only) were seen at 3000 and 8000 ppm and decreases in brain and spleen weights were also noted (the latter decreases were without microscopic lesions and occurred at 8000 ppm only). An increase in hepatocellular hypertrophy occurred in both sexes at the two highest concentrations. The only neoplastic lesion found in this study in mice was an increased incidence of hepatocellular adenomas in females at the 8000 ppm exposure. In a follow-up study, a statistically significant elevation of cell proliferation in female mouse liver has been shown to occur following 5 days, but not 28 days, of exposure to 8000 ppm MTBE, suggesting that MTBE induces mitogenesis. For male rats, early euthanasia was required at week 82 and week 97 for the 8000 and 3000 ppm groups, respectively, due to excessive mortality from a severe progressive nephrosis. The end stage of this process appeared earlier in the male rats of all MTBE exposure groups; the incidence of this lesion and mortality for exposed females was comparable to control females. No exposure-related changes in hematological parameters were observed for any group at any time point, but a decrease in corticosterone levels was seen for male rats from the 8000 ppm group. Absolute and relative kidney and liver weight increases occurred in 3000 and 8000 ppm exposure groups, but the liver weight change was not accompanied by histopathological change. At study termination, increases in the incidence and severity of a chronic nephropathy in males from all exposure groups and in females exposed to 3000 and 8000 ppm was associated with secondary lesions of hyperplasia of the parathyroid and mineralization of tissues. Renal tubular cell tumors were increased in male rats exposed to 3000 and 8000 ppm. This may be associated with an accumulation of protein (stainable by Mallory's Heidenhain) in kidney tubular epithelial cells after 4 weeks of exposure. An increased incidence of interstitial cell adenomas of the testes was seen in males exposed to 3000 and 8000 ppm but was believed to be an artefact of an unusually low control incidence and not considered to be exposure related. Based on the above effects, the no-observed-effect level (NOEL) for chronic toxicity is 400 ppm, and the NOEL for carcinogenic effects is 3000 ppm (mice) and 400 ppm (rats).
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PMID:Oncogenicity studies of inhaled methyl tertiary-butyl ether (MTBE) in CD-1 mice and F-344 rats. 917 27

Glomerular function and structure were serially evaluated in 15 patients with membranous nephropathy who exhibited relapsing nephrosis and chronic depression of GFR. GFR declined from 56+/-8 (mean+/-SEM) at onset to 31+/-4 ml/min per 1.73 m2 after a 2- to 5-yr period of observation (P < 0.05). An analysis of filtration dynamics suggested persistent elevation of net ultrafiltration pressure. To examine a possible role for declining intrinsic glomerular filtration capacity as the basis for the observed hypofiltration, glomeruli in the baseline and a repeat biopsy (performed after a median of 28 mo) were subjected to morphometric analysis and mathematical modeling. Analysis of the baseline biopsy revealed a reduction in filtration slit frequency and thickening of the glomerular basement membrane, lowering computed hydraulic permeability by 66% compared with normal kidney donors. In contrast, filtration surface area was increased by 37% as a result of glomerular hypertrophy. The repeat biopsy revealed persistent depression of hydraulic permeability, primarily owing to foot process broadening. An additional finding was a decrease in filtration surface area from baseline in patent glomeruli, possibly due to encroachment on the capillary lumen of an increasingly widened basement membrane. Also, a striking increase in the prevalence of global glomerulosclerosis from 7+/-2% to 23+/-4% was found between the two biopsies, suggesting a significant loss of functioning nephrons. It is concluded that hypofiltration in membranous nephropathy is the consequence of a biphasic loss of glomerular ultrafiltration capacity, initially owing to impaired hydraulic permeability that is later exacerbated by a superimposed loss of functioning glomeruli and of filtration surface area.
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PMID:Mechanisms of progressive glomerular injury in membranous nephropathy. 969 60

On December 29 1995, a 13-year old, male Spanish ibex was easily captured by hand, with depression, weakness and severe tick infestation, mainly in the periocular and auricular regions. Blood and serum samples were collected and haematological analysis and serum iron levels were determined. Red blood cell count, haematocrit, haemoglobin concentration and mean corpuscular haemoglobin concentration (MCHC) were decreased and mean corpuscular volume (MCV) increased (macrocytic-hypochromic anemia). Serum iron and transferrin saturation were decreased and total and unbound iron-binding capacity were increased. Piroplasms were observed within parasitized erythrocytes and presumptively identified as Babesia spp. Ticks were identified exclusively as Ripicephalus bursa. The animal was treated with imidocarb but died after 15 days of capture. Histopathological examination revealed congestion of pulmonary capillaries and spleen, glomerulonephritis, hemoglobinuric nephrosis and generalized hemosiderosis. An indirect fluorescent antibody test was performed using a Babesia ovis isolate of ovine origin as antigen and the animal was positive with a titre of 1:640.
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PMID:Presumptive Babesia ovis infection in a spanish ibex (Capra pyrenaica). 1062 13

Sediment ingestion has recently been identified as an important exposure route for toxicants in waterfowl. The effects of lead-contaminated sediment from the Coeur d'Alene River Basin (CDARB) in Idaho on posthatching development of Canada geese (Branta canadensis) were examined for 6 wk. Day-old goslings received either untreated control diet, clean sediment (48%) supplemented control diet, or CDARB sediment (3449 microg/g lead) supplemented diets at 12%, 24%, or 48%. The 12% CDARB diet resulted in a geometric mean blood lead concentration of 0.68 ppm (ww), with over 90% depression of red blood cell ALAD activity and over fourfold elevation of free erythrocyte protoporphyrin concentration. The 24% CDARB diet resulted in blood lead of 1.61 ppm with decreased hematocrit, hemoglobin, and plasma protein in addition to the effects just described. The 48% CDARB diet resulted in blood lead of 2.52 ppm with 22% mortality, decreased growth, and elevated plasma lactate dehydrogenase-L (LDH-L) activity. In this group the liver lead concentration was 6.57 ppm (ww), with twofold increases in hepatic lipid peroxidation (thiobarbituric acid-reactive substances, TBARS) and in reduced glutathione concentration; associated effects included elevated glutathione reductase activity but lower protein-bound thiols concentration and glucose-6-phosphate dehydrogenase (G-6-PDH) activity. The kidney lead concentration in this group was 14.93 ppm with subacute renal tubular nephrosis in one of the surviving goslings. Three other geese in this treatment group exhibited calcified areas of marrow, and one of these displayed severe chronic fibrosing pancreatitis. Lead from CDARB sediment accumulated less readily in gosling blood and tissues than reported in ducklings but at given concentrations was generally more toxic to goslings. Many of these effects were similar to those reported in wild geese and mallards within the Coeur d'Alene River Basin.
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PMID:Developmental toxicity of lead-contaminated sediment in Canada geese (Branta canadensis). 1070 32


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