Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although plants containing hydrolysable tannins can be hepatotoxic, such poisoning has not been reported in Indonesia despite the presence of these plants. In order to determine the hepatotoxic potential of Indonesian plants, goats were intoxicated experimentally with the Indonesian plant Climedia hirta (harendong), which contained 19% hydrolysable tannin. The prophylactic effect of Ca(OH)2 supplementation on the disease was also examined. Two groups of goats were fed for 28 days with grain-based pellets containing 50% harendong leaf or 50% harendong leaf + 8% Ca(OH)2. Two control groups were fed similar pellets containing 50% of the non-toxic elephant grass (Pennisetum purpureum) with and without 8% Ca(OH)2. Serum enzymes indicative of liver damage were monitored during the experiment and histopathological examination of selected tissues was done at the conclusion of the experiment. In goats given unsupplemented harendong pellets there was a significant increase in aspartate aminotransferase and glutamate dehydrogenase from 50.2 and 20.6 U l-1 to 219.6 and 63.3 U l-1, respectively. These changes were associated with moderate to severe nuclear plemorphism, vacuolation and megalocytosis of hepatocytes and deposits of brown pigment in the Kupffer cells. There was also nephrosis of the renal convoluted tubules and collecting ducts, abomasitis and enteritis. Biochemical and histological changes were reduced significantly in the harendong + Ca(OH)2 group and virtually absent from control groups. It is concluded that hydrolysable tannins in harendong leaf are hepato- and nephrotoxic and associated with gastroenteritis, but that poisoning may be ameliorated by Ca(OH)2 supplementation.
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PMID:Prevention of hydrolysable tannin toxicity in goats fed Clidemia hirta by calcium hydroxide supplementation. 225 83

In a 106-wk toxicity and carcinogenicity study, groups of 60 male and 60 female weanling Wistar rats were fed 0, 0.5, or 50 mg bis(tri-n-butyltin)oxide (TBTO)/kg diet. In males, feed consumption was increased in all treated groups and increased water consumption occurred at 5 and 50 mg/kg. During the second year, body weight decreased in the 50-mg/kg males, while the females in that group showed no weight gain. Excess mortality was confined to the 50-mg/kg group towards the end of the study. Haematological changes, comprising anaemia, lymphocytopenia and thrombocytosis were noted mainly at the high-dose level. Also, signs of decreased kidney function and increased plasma enzyme activities (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) were noted. No effects on serum hormone concentrations (thyrotropin, follicle stimulating hormone, luteinizing hormone or insulin) were observed, except for a decrease in the free thyroxin:thyroxin ratio in both sexes at the high-dose level. Higher serum IgM and IgA levels were present at 50 mg/kg, while, in females, IgG was decreased. At 50 mg/kg, the ovaries, adrenals, spleen (females), heart (males), pituitary, liver and kidneys were increased in weight, but the thyroid weight was decreased in females. The total tin concentrations in liver and kidneys showed a dose relationship and, in general, the concentrations were similar after 1 and 2 yr. Non-neoplastic histological alterations after 1 yr consisted of a decrease in the cell height of the thyroid follicles in all dose groups, with a reduced number of psammoma bodies at 50 mg/kg, a decrease in splenic iron content at 5 (females only) and 50 mg/kg, and a slight bile-duct activation. After 2 yr, only the thyroid changes were still present. In addition, at 2 yr, vacuolation and pigmentation of the proximal tubular epithelium and nephrosis were enhanced at 50 mg/kg. The incidence of benign tumours of the pituitary was significantly elevated and enhanced at 0.5 and 50 mg/kg. At 50 mg/kg increases in pheochromocytomas in the adrenal medulla and in parathyroid adenomas (males) were noted, while adrenal cortical tumours were decreased (males). There was a low, non-dose-related incidence of pancreatic carcinoma. Other tumour rates were in line with control data. It is concluded that lifetime feeding of 50 mg TBTO/kg diet induces toxicity in various organ systems. An increase in some common tumours was found at the high dose, probably due to hormonal or immunological changes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic toxicity and carcinogenicity of bis(tri-n-butyltin)oxide (TBTO) in the rat. 234 92

To examine the effects of acute exposure to fumonisin-containing culture material (FCCM), 15 crossbred wether lambs were dosed intraruminally with FCCM containing 0 (CONTROL, n = 3), 11.1 (LOW, n = 4), 22.2 (MED, n = 4), or 45.5 (HIGH, n = 4) mg of total fumonisins (B1, B2, and B3)/kg BW daily for 4 d. Blood samples were collected daily, and on d 11 lambs were killed and necropsied. Changes in serum constituents in fumonisin-treated lambs indicative of liver damage, included increased (P < .05) activities of alkaline phosphatase, gamma-glutamyl transferase, aspartate aminotransferase, and lactate dehydrogenase. Serum concentrations of cholesterol, triglycerides, urea nitrogen, and creatinine were also increased (P < .05) in lambs dosed with FCCM. Hemoglobin tended to increase (P = .07) and white blood cell count tended to decrease (P = .08) in HIGH lambs and activated partial thromboplastin time tended to decrease (P < .10) in lambs dosed with LOW and MED treatments. Mitogen-induced lymphocyte blastogenesis was not different (P = .14) among treatments. Feed intake markedly decreased (P < .01) following the first dosing of FCCM and continued to decline throughout the study. Ruminal VFA concentrations and pH tended to decrease (P < .10) at d 11 in treated lambs. Relative liver and kidney weights (g/100 g of BW) increased (P < .05) in fumonisin-treated lambs. Histiolgical examination revealved tubular nephrosis and mild hepatopathy in dosed lambs. Lambs receiving the HIGH treatment died on d 3, 4, 5, and 7 of the study and on d 9 one lamb on the MED treatment died.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute hepatic and renal toxicity in lambs dosed with fumonisin-containing culture material. 760 85

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

Aflatoxin (AF)-contaminated and fumonisin B1 (FB1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of AF and 0 mg of FB1/kg of feed (control); 2.5 mg of AF/kg of feed; 100 mg of FB1/kg of feed; or 2.5 mg of AF plus 100 mg of FB1/kg of feed for 35 days. The effects on production performance, serum biochemical, hematologic, immunologic, and pathologic measurements were evaluated. Body weight, gain, and feed consumption were significantly (P < 0.05) decreased by AF and AF plus FB1 diets. The FB1 diet decreased feed consumption, and although body weight was numerically decreased, it was not statistically significant. Aflatoxin increased serum gamma-glutamyltransferase (GGT) activity and total iron concentration and decreased urea nitrogen concentration and unsaturated iron-binding capacity. The FB1-alone diet increased serum GGT activity, whereas the AF plus FB1 diet increased serum aspartate transaminase, cholinesterase, alkaline phosphatase, and GGT activities, increased RBC count, triglycerides, and total iron concentrations, and decreased unsaturated iron-binding capacity and urea nitrogen concentration. For the most part, the effects of the AF plus FB1 diet on body weight and hematologic measurements could be considered additive. However, the effect of the AF plus FB1 diet on cholinesterase and alkaline phosphatase activities was greater than additive and was a synergistic response. One pig in the FB1-diet group and 2 pigs in the combination-diet group died. Postmortem lesions in pigs of the FB1-diet group consisted of ascites and increased liver weight. Observations at necropsy for pigs of the AF plus FB1-diet group consisted of hydrothorax, ascites, pulmonary edema, gastric erosions and ulceration, and increased liver and spleen weights. The AF diet increased relative liver weight and resulted in liver that was pale, rubbery, and resistant to cutting. Histologic lesions consisted of hepatic necrosis or degeneration, or both, with variable degrees of bile duct proliferation in barrows of the AF-diet groups. Renal tubular nephrosis was observed in barrows of the FB1-diet group, but this was not consistent in the AF plus FB1-diet group. Cell-mediated immunity, as measured by mitogen-induced lymphoblastogenic stimulation index, was decreased in barrows of the AF and FB1-diet groups, and values in barrows given the combination diet were significantly decreased from those in barrows given the single toxin diets. It was concluded that AF and FB1 (from culture material), singly or in combination, can adversely affect clinical performance, serum biochemical, hematologic, and immunologic values and induce lesions in growing barrows. For most of the variables we evaluated under our study conditions and dosages of toxins, measurements were affected more by the combination diet than by either single toxin diet, and the toxic responses could be described as additive or more than additive, particularly for induction of liver disease.
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PMID:Influence of aflatoxin and fumonisin B1-containing culture material on growing barrows. 859 31

Aminoglycoside antibiotics are indispensable for treatment of serious bacterial infections, and despite careful attention to dosage regimens, nephrotoxicity and ototoxicity still cause concern. In the present study, we tested whether side effects of aminoglycoside therapy could be limited by expression of prokaryotic genes of antibiotic resistance in vivo. We characterized the acute and tissue-specific toxicity of hygromycin B in transgenic mice bearing the hygromycin B phosphotransferase (hygR) gene under control of a constitutive promoter. We characterized the tissue-specific expression of hygR mRNA and also investigated the acute toxicity of hygromycin B in hygR and wild-type mice. The hygR mRNA reached its highest levels in brain and reached intermediate levels in spleen, muscle, kidney, liver and testis. The lowest levels were detected in heart and lungs. The hygR expression in transgenic animals caused an 89-fold increase in the approximate lethal dose of hygromycin B compared with wild-type mice. Serum biochemical analysis of hygR and wild-type mice treated with lethal doses of hygromycin B indicated liver and kidney damage measured as ALT, AST and BUN. On the morphological level, these changes led to acute tubular nephrosis in wild-type mice and acute liver damage in hygR mice. Our results show that constitutive expression of the bacterial hygR gene in transgenic mice in vivo confers resistance to hygromycin B.
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PMID:Expression of hygR in transgenic mice causes resistance to toxic effects of hygromycin B in vivo. 915 10

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D), a herbicide, was studied in chicks dosed with 100, 300, 500, or 600 mg 2,4-D/kg BW, by the oral route. Clinical, laboratory, and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased motor activity and induced muscular weakness and motor incoordination; decreased weight gain; increased serum creatine kinase (CK) and alkaline phosphatase (AP) activities and serum uric acid (UA), creatinine (CR), and total proteins (TP) levels; and did not change serum aspartate aminotransferase (AST) or alanine aminotransferase (ALT) activities. These changes were time- and dose-dependent and reversible. The LD50 (lethal dose 50%) calculated for oral 2,4-D in chicks was 420 mg/kg BW (385 to 483). Chromatographic analysis of the serum of the intoxicated chicks showed the presence of the herbicide; the amount found was dose- and time-dependent, increasing from 2 to 8 h after exposure and decreasing afterwards. Histopathological post-mortem studies conducted on intoxicated chicks showed hepatic (vacuolar degeneration of the hepatocytes), renal (tubular nephrosis), and intestinal (hemorrhagic) lesions. Taken together, the observed alterations mainly reflected kidney and muscle tissue damage, although hepatic toxicity may also have occurred after acute 2,4-D intoxication.
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PMID:Acute 2,4-dichlorophenoxyacetic acid intoxication in broiler chicks. 956 31

A probable outbreak of oak (Quercus calliprinos) toxicosis in a herd of beef cattle--heifers and first-calving cows--grazing in the Judean foothills of Israel is described. Toxicosis probably occurred because of the consumption of oak leaves and buds during a period of pasture scarcity without any feed supplementation. A progressive syndrome of wasting, dullness, anorexia, polyuria, nephrosis, constipation and recumbency, culminating in death, was seen. A high mortality rate of 83% (38/46 animals) was noted. The clinical-pathological findings revealed increases in blood urea, creatinine, aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), creatine kinase (CK), lactate dehydrogenase (LDH) and inorganic phosphorus. Decreases were found in alkaline phosphatase (ALP), total serum protein, albumin (ALB), triglyceride (TG), calcium (Ca), magnesium (Mg), sodium (Na) and chloride (CI). The main pathological findings were severe nephrosis, chronic interstitial nephritis, and occasional intestinal ulceration. On the basis of epidemiology, clinical signs, clinical-pathological and pathological findings and renal histology, a tentative diagnosis of oak toxicosis was made.
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PMID:Probable toxicosis in cattle in Israel caused by the oak Quercus calliprinos. 983 Jun 93

In this study the short term (3 months) toxicological effects of varying levels of Catha edulis leaves were examined on the plasma concentration of liver enzymes and the histopathology of tissue sections of various organs including the liver, kidneys, spleen and testis. Both the biochemical and histopathological data demonstrated, initial signs of Catha edulis toxicity. Our results show a significant increase in plasma levels of alkaline phosphatase (ALP) and alanine aminotransferase (ALT) with all levels of Catha edulis leaves tested and throughout the treatment period. The increase of ALP was more prominent than that of ALT. The plasma levels of aspartate aminotransferase (AST) were only moderately increased at the higher dose (30%) in the later stages of treatment. In addition, a time-dependent gradual increase in indirect bilirubin with a concomitant decrease in direct bilirubin levels was observed with the 30% Catha edulis with no signs of haemolysis. The histopathology of tissue sections of the liver displayed evidence of congestion of the central liver veins as well as acute hepatocellular degenerative and regenerative activities in the tissue sections obtained from animals treated with both 20% and 30% Catha edulis. Similarly, histopathological examination of the tissue sections of the kidneys showed some lesions, and the degree of the lesion increased as the dose of Catha edulis leaves increased including: the presence of fat droplets particularly seen in the upper cortical tubules; acute cellular swelling; hyaline tubules; and acute tubular nephrosis. In contrast, Catha edulis treatment did not affect the spleen and increased the rate of spermatogenesis in male rabbits with the spermatozoa being quite evident, the Leydig cells were in good condition and were not affected by the doses given.
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PMID:Investigation into the toxicological effects of Catha edulis leaves: a short term study in animals. 1193 13

Chloroform extract of Prunus africana (Hook f. (Rosaceae) did not cause clinical signs or pathology in rats at daily oral doses of up to 1,000 mg/kg for 8 weeks. The extract caused marked clinical signs, organ damage and a 50% mortality rate at a dose of 3.3 g/kg for 6 days. The main lesions observed at this dose were marked centrilobular hepatocellular degeneration and necrosis, diffuse nephrosis, myocardial degeneration, lymphocytic necrosis and neuronal degeneration. The morphological damage in these tissues caused a corresponding rise in blood biochemical parameters namely, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, creatine kinase and blood urea nitrogen. The target organs of toxicity of this extract are the liver, kidney and heart. Overt toxicity occurred only after the administration of multiple doses of 3.3 g/kg body weight. These findings confirm the suitability of this extract for therapeutic use, since the doses used in the therapy of prostate gland are much lower than those used in this study and would therefore not be expected to cause pathological changes.
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PMID:Toxicity of chloroform extract of prunus africana stem bark in rats: gross and histological lesions. 1216 69


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