Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

d.d-T80-prallethrin, a pyrethroid insecticide for sanitary use, was administered to Crj : CD (Sprague Dawley) rats at concentrations of 120, 600 or 3,000 ppm in diet for one year to assess the chronic toxicity potential and the reversibility. The summarized results obtained are as follows: 1. Chronic toxicity study 3,000 ppm : Decreases in body weight gain, food consumption, and water intake were observed. Slight alopecia in the neck and/or back was noticed during the first and second weeks, but the animals were recovered thereafter. Slight anemic changes such as decreases in hemoglobin concentration, hematocrit value, MCV and MCH were observed in the females at 52 week. Blood biochemistry revealed increases in total cholesterol (in the males and females at 13, 26 and 52 weeks), phospholipid (in the males and females at 13, 26 and 52 weeks), albumin (in the males at 13 and 26 weeks, in the females at 52 week), total protein (in the males at 26 week, in the females at 52 week), A/G ratio (in the males at 13 week, in the females at 26 week), creatinine (in the males at 52 week), urea nitrogen (in the females at 52 week), GOT (in the males and females at 52 week) and GPT (in the males and females at 52 week), and decreases in triglyceride (in the females at 26 and 52 weeks) and alkaline phosphatase (in the males at 13 and 52 weeks). In urinalysis, an increase in bilirubin was observed in the males at 52 week. Gross-pathology revealed a lower incidence of accentuated lobular pattern of liver (in the males at 26 week) and a higher incidence of enlarged liver (in the males at 52 week). In organ weight, increases in liver (in the males and females at 26 and 52 weeks), kidney (in the males at 26 and 52 weeks) and thyroid weights (in the males at 26 and 52 weeks, in the females at 26 week), and decreases in spleen (in the females at 26 and 52 weeks) and adrenal weights (in the females at 52 week) were observed. Histopathological examination revealed a lower incidence of fatty metamorphosis in the liver of females at 52 week. 600 ppm: An increase in liver weight was observed in the males at 26 week. 120 ppm: No effect was observed. 2. Reversibility study Almost all the above chronic toxicities were reversible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[One-year chronic dietary toxicity study of d.d-T80-prallethrin in rats]. 344 42

Fourteen goat fetuses were totally sustained in water by extracorporeal perfusion using a membrane oxygenator. The two groups which underwent perfusion methods may be described as follows: One was an A-V bypass through umbilical vessels which has been reported previously, and the other was a new method, a V-A bypass through cervical vessels. Ten fetuses were perfused by an A-V bypass and the longest survival time was 9 hours. Three fetuses suddenly died shortly after perfusion was started. Four fetuses were perfused by a V-A bypass and the longest survival time was 27 hours. Cardiovascular dynamics were stable from the beginning of perfusion. Autopsy revealed hepatomegaly and bloody ascites in A-V bypassed fetuses but not in the fetuses perfused by a V-A bypass. The A-V bypass through umbilical vessels resembles physiological fetal circulation, and the cannulation technique is not difficult but it needs strict control, especially in the early stages of perfusion. A V-A bypass through cervical vessels doesn't seem to be close to a physiological perfusion for fetuses and the cannulation technique is difficult. But the cardiovascular dynamics are stable, so they are employed for clinical uses in neonatal ECMO. The V-A bypass method seems to be an adequate technique for managing extremely premature fetuses in water.
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PMID:[Management of the goat fetus in water using membrane oxygenator by V-A bypass through the cervical vessels--comparison with the A-V bypass method through umbilical vessels]. 358 6

Experiments were conducted to study the total lipid and fatty acid composition of liver, kidney, brain and heart of 7-wk-old male C57BL mice. Dietary copper deficiency was initiated at birth by feeding dams a purified diet containing 0.5 mg/kg copper. Offspring were fed the copper-deficient diet 4 wk postweaning. Control dams and offspring were fed the same diet but with added copper in the drinking water, 20 mg/L. Compared with controls the copper-deficient mice exhibited hepatomegaly, cardiac hypertrophy and a 4% reduction in brain weight as well as low ceruloplasmin activity (0.5% of control). Total phospholipid concentration in liver and kidney and total triacylglycerol concentration in kidney was lower in copper-deficient mice compared to concentrations measured in liver and kidney of control mice. The major change in essential fatty acid composition in the copper-deficient mice which was consistent between organs and lipid classes was a significantly lower proportion and absolute amount of dihomo-gamma-linolenic acid. Other changes in fatty acid composition were variable.
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PMID:Lipid and fatty acid composition of organs from copper-deficient mice. 374 62

The progression of aflatoxicosis was evaluated in young broiler chickens (Hubbard X Hubbard). The experimental design consisted of four dietary treatments of aflatoxin (0, 1.25, 2.5, and 5.0 micrograms of aflatoxin/g of feed, ppm) and 11 replicates of 10 broilers/replicate. The broilers were maintained in electrically heated batteries with feed and water available ad libitum from hatching to 3 weeks of age. The broilers were weighed, bled, killed by cervical dislocation, and necropzied at 3, 6, 9, 12, 15, 17, and 21 days of age. Body weights were significantly decreased by 5.0 ppm aflatoxin at 6 days of age and by 2.5 ppm at 17 days of age. Aflatoxin induced a significant increase in the relative weight of the proventriculus, gizzard, spleen, and kidney. Liver atrophy was indicated in the early stages of aflatoxicosis by a decrease in the relative weight of this organ. As aflatoxicosis progressed, hepatomegaly became apparent due to lipid accumulation in the liver. Packed-cell volume and hemoglobin levels were significantly decreased by 5.0 ppm aflatoxin at 12 days and by 2.5 ppm aflatoxin at 21 days of age. Serum levels of albumin and total protein were significantly reduced at 5.0 and 2.5 ppm aflatoxin by 3 and 6 days of age, respectively. Serum levels of uric acid, triglycerides, and cholesterol were significantly decreased from control values from 12 through 21 days of age by 5.0 ppm aflatoxin and, to a lesser extent, by 2.5 ppm aflatoxin. The activity of serum lactic dehydrogenase was significantly decreased at all aflatoxin treatment levels from 12 through 21 days of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Progression of aflatoxicosis in broiler chickens. 379 71

Cyclohexanone oxime (CHO) was given po to male and female Fischer 344 rats at dose levels of 10, 25, 75, 150, and 300 mg/kg, five times a week for a period of 2 weeks. Control animals received distilled water. All animals given intermediate dose levels (10, 25, 75, and 150 mg/kg) and one half of the animals which were dosed at the high dose (300 mg/kg) as well as one half of the controls were terminated 14 days after administration of the first dose. The remaining rats received no treatment for an additional 14 days and were sacrificed on Day 28 of the study (recovery phase). Dose-related decreases in erythrocyte number, hemoglobin, and hematocrit, with an accompanying increase in reticulocytes and circulating nucleated erythrocytes, were observed in both sexes at Day 14. Methemoglobin levels, determined only at the high dose, were elevated in both sexes at this time. Splenomegaly and hepatomegaly were observed in both sexes at 14 and 28 days. Histopathological examination of the spleen and bone marrow revealed dose-related erythroid hyperplasia at 14 days which subsided by Day 28. The above effects were more pronounced in males. Erythrocyte numbers were only slightly depressed and reticulocytes mildly elevated in males at Day 28. Hematological values were not statistically different from controls in females at this time. These results suggest that CHO induces oxidative damage to the erythrocyte, resulting in a hemolytic anemia accompanied by increased erythropoiesis. The toxic effects appear reversible upon cessation of exposure.
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PMID:Toxicity of cyclohexanone oxime. I. Hematotoxicity following subacute exposure in rats. 398 89

A girl presented with an important growth retardation, hepatomegaly, fasting hypoglycemia, lactic acidosis, increased serum cholesterol, triglycerides and uric acid, and increased liver glycogen (7.5%). There was no rise in blood glucose after IV galactose or fructose, but glucagon gave a delayed response. Type Ib glycogen storage disease was suggested by the low normal activity of glucose-6-phosphatase (G-6-Pase) which reached 1.8 units/g (normal, 2 to 10 units/g) and the normal activity of other glycogenolytic enzymes, measured in homogenates prepared in H2O (mean +/- S.E. in control subjects: 59% +/- 7; in type Ia GSD: 92% +/- 3). The activity of G-6-Pase measured as described above increased to 3.8 units/g of liver 1 year after PCS and 7.85 units/g of liver after 3 years. At that time, a simultaneous assay of the enzyme in a fresh, previously not frozen liver biopsy, homogenized in 0.25 M sucrose, revealed only about 29% of the activity of the same sample prepared in H2O (mean +/- S.E. in three controls: 95.8% +/- 8.9.
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PMID:Clinical and biochemical findings before and after portacaval shunt in a girl with type Ib glycogen storage disease. 625 80

To study the role of endothelial damage in the pathogenesis of lung injury induced by the pyrrolizidine alkaloid monocrotaline, three functions (angiotensin converting enzyme (ACE) activity, plasminogen activator (PLA) activity, and prostacyclin (PGI2) production) associated with the pulmonary endothelium were examined, and were correlated with pulmonary arterial perfusion and ultrastructure in rats receiving monocrotaline in their drinking water (20 mg/liter) for 1-12 weeks. Lung ACE activity increased after 1 week of monocrotaline, then decreased steadily from 1 to 6 weeks, before plateauing at approximately 55% of normal. PLA activity in monocrotaline-treated lungs did not change significantly for the first 2 weeks, then decreased to 59 and 79% of the control value after 6 and 12 weeks, respectively. In contrast, PGI2 production increased progressively, reaching 140 and 270% of the control level after 6 and 12 weeks of monocrotaline treatment, respectively. These endothelial functional changes were not accompanied by significant changes in pulmonary arterial perfusion as visualized by 99mTc lung scans. Electron microscopy of monocrotaline-treated lungs revealed endothelial damage (perivascular and subendothelial edema, degeneration) starting at 1 week, and inflammatory and hemorrhagic reactions starting at 2 weeks. At 6 and 12 weeks, monocrotaline-treated rats also exhibited increased pulmonary arterial wall thickness, right heart enlargement, and cardio- and hepatomegaly. Thus, monocrotaline-induced pulmonary injury is accompanied, and in some cases preceded, by structural and functional abnormalities in the pulmonary endothelium.
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PMID:Monocrotaline-induced pulmonary endothelial dysfunction in rats. 632 29

Glucocorticoid treatment in dogs is known to cause hepatocellular swelling due to accumulation of cytoplasmic compounds which variably have been identified histochemically as fat, glycogen, or water. In the present study changes in dog liver, after treatment for 15 days with two different doses of oral or intramuscular prednisone, were examined using histological, histochemical, and ultrastructural techniques as well as quantitative chemical analysis. Thirty mongrel dogs were divided into two control groups and three treatment groups of six dogs each. Dogs which received prednisone orally at 1.2 mg/kg body weight/day, or 4 mg/kg body weight/day, respectively, or received intramuscular prednisone injections of 4 mg/kg body weight/day had hepatomegaly due primarily to hepatocellular accumulation of glycogen. Compared to controls, no changes in the hepatic water concentration were observed, whereas the relative amounts of liver fat were decreased slightly and those of protein were decreased markedly. Hepatocellular glycogen could be demonstrated histochemically in tissues fixed in absolute alcohol, but not in tissues treated with aqueous fixative, such as 10% buffered formalin or Bouin's solution. Glycogen deposition occurred predominantly in the midzone of hepatic acini. Affected hepatocytes varied in size and shape. The most severely affected cells were enlarged five to ten fold with glycogen occupying most of the cytoplasmic space restricting the mitochondria, endoplasmic reticulum, and other organelles to a narrow zone around the cell periphery and the nucleus. It was concluded that treatment with prednisone causes hepatomegaly due to glycogenosis in the dog.
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PMID:Prednisone-induced morphologic and chemical changes in the liver of dogs. 646 1

It has been estimated that there are some 30,000 chemical waste dumps in the United States. Many of these landfill operations were undertaken in the early 1950s and 1960s, when knowledge regarding the safe and prolonged containment of the waste buried was nonexistent or minimal at best. As a result, many of these dump sites were located in areas that were geologically unsuitable for toxic chemical wastes. The Love Canal area in Niagara Falls, NY, is probably the best known of these dump sites. While a few of these sites have attracted wide media coverage, the availability of objective scientific information regarding the health effects of such sites has been deficient. The present study of a large toxic waste dump located in Hardeman County, TN, its contamination of surface and underground aquifers and the health effects on the area residents exposed via ingestion of contaminated water, offers the first objective evidence of organ dysfunction in such a human population. During this study comprehensive evaluation of that population revealed multiple symptoms, evidence of hepatomegaly and elevated liver function tests apparently caused by ingestion of water contaminated by numerous organic chemicals, many of which are known to be hepatotoxins.
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PMID:Liver dysfunction in residents exposed to leachate from a toxic waste dump. 682 41

Ground water that was used as a source of potable water by residents of a small community became contaminated by leachate from a 300,000 barrel pesticide waste dump. An environmental health survey of the residents and an apparent control group was conducted to determine if any adverse health effects resulting from exposure to the toxic compounds, many of which were hepatotoxins, could be detected. The survey utilized a health questionnaire, a clinical examination, and a biochemical screening. The latter included analysis of serum for liver and kidney function parameters, determination of hepatitis A and B serology, and bile acid determinations on fasting and postprandial serum and urine specimens. Air and water from representative homes and urine from study participants were analyzed for selected organic compounds. The biochemical screening was conducted on two occasions 2 months apart. The initial hepatic profile testing revealed elevated concentrations of the serum enzymes, alkaline phosphatase and serum glutamic oxaloacetic transaminase, in residents who had used the contaminated water. During follow-up testing of these same persons 2 months later, these values were significantly reduced, as were postprandial serum concentrations of the bile acid of cholyglycine. Six individuals in the exposed group had slight hepatomegaly compared to one individual in the intermediate exposure group and none in the controls. Concentrations of carbon tetrachloride were as high as 18,700 microgram/L in the well water samples. The biochemical and clinical observations are suggestive of a transitory liver injury probably related to exposure to the contaminated drinking water.
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PMID:An environmental health survey of drinking water contamination by leachate from a pesticide waste dump in Hardeman County, Tennessee. 705 35


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