Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum activity analyses of nine enzymes [CPK, HBDH, SDH, ALP, GPT, GOT, LDH, MDH, ALD] in patients with rheumaitc carditis revealed certain elevations of the mean values of LDH, GOT, HBDH, GPT, ALP and MDH. These changes have no particular diagnostic importance because similar findings were also obtained in patients with both rheumatic and nonrheumatic arthritis. The changes occurring during antirheumatic treatment are minimal and statistically not significant. Greater elevations of LDH, ALD, GOT, HBDH, GPT, MDH, and ALP are found in patients with decompensated rheumatic heart disease associated with active rheumatic carditis.
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PMID:Changes in blood-serum enzymes in rheumatic myocarditis. 102 12

Serum GOT, GPT, LDH, CHE, MDH, SDH, PK, GLDM, LAP and amylase levels and serum ammonia were determined in 49 major burn cases with 2nd and 3rd degree lesions covering 25% to 80% of the body surface. GOT, GPT, LDH, CHE and gamma-GT have above normal in all cases. Limited and inconsistent movements were noted for the remaining enzymes. Blood ammonia was constantly increased and it is felt that the enzyme picture may be of considerable prognostic value in major burn cases.
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PMID:[Serum enzyme picture in major burns]. 111 73

The authors report on occurrence, causes and diagnostics of liver affections observed in fattening bulls in Ukrainia between 1982 and 1988. For this purpose, 2747 bulls in 10 fattening plants had been controlled clinically once during the last month of their final fattening period (lasting, according to the feeding schedule, from the 4th until the 12th, or from the 6th until the 18th month of life), and 1318 of them were controlled for eventual hepatic lesions at slaughter. The authors found an increase in liver affections during the final fattening period. The type of lesion found preferentially in the different fattening plants showed a certain correlation with feeding used in these: The prevalence of liver lesions (i.e. in 87.2% of the animals controlled) were found in fattening bulls fed cereal branstraw-pellets; among these, liver abscesses were most frequent (i.e. 55.2% of all lesions observed in this group). Steatosis of the liver was prevalent in fattening bulls receiving eating offalls (i.e. 82.7% of all lesions found in that group), whereas liver cirrhosis was prevalent in fattening bulls fed with sugar beet chips-silage. In Holstein-bulls, liver lesions were about double as frequent as in Fleckvieh-bulls (i.e. 37.3 and 16.7% of the livers controlled were found involved, respectively). Diagnostical value of several clinical parameters controlled is discussed (i.e. size and sensitivity of liver percussion field, activity of SDH, LDH, AST and ALT in serum, serum concentration of vitamin A, D3-25 and E, concentration of Vitamin A in liver, and concentration of cholic acids and of their glucoconjugates in bile).
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PMID:[Liver diseases of fattening bulls]. 150 64

It has been shown that BrCCl3 is a more potent hepatotoxin than CCl4. Pretreatment with nontoxic dietary levels of chlordecone (CD) results in amplification of BrCCl3 hepatotoxicity. The objective of this research was to investigate and compare the histopathological alterations during a time course after a low dose of BrCCl3 alone and in combination with dietary CD. Male Sprague-Dawley rats were maintained on 10 ppm dietary CD or normal diet for 15 days. On day 16, they received a single ip dose (30 microliters/kg) of BrCCl3 in corn oil (CO) vehicle or corn oil alone. Blood and liver samples were collected at 0, 3, 6, 12, 24, 36, 48, 72, 96, and 120 hr for serum enzymes and histopathological examination, respectively. Serum enzymes (SDH, ALT, AST) were significantly (p less than 0.05) elevated in rats receiving the CD + BrCCl3 combination in comparison to BrCCl3 alone. For 48 hr, a continuous increase in serum enzyme activities was detected in rats treated with CD + BrCCl3 combination, but not in the rats receiving other treatments (ND + BrCCl3, ND + CO, or CD + CO). The most extensive hepatolobular necrosis was observed in rats treated with the CD + BrCCl3 combination. Thirty-six hr after the administration of BrCCl3 to rats maintained on normal diet, high mitotic activity was observed, which continued through 72 hr resulting in complete restoration of hepatolobular structure. In contrast, rats receiving the combination of CD + BrCCl3 exhibited minimal and belated hepatomitotic activity for a short period of time, resulting in progressive hepatic failure, culminating in animal death. In conclusion, hepatotoxicity of a low dose of BrCCl3 alone appeared to be overcome via stimulated hepatocellular regeneration and hepatolobular restoration. CD appears to amplify BrCCl3 hepatotoxicity via interference with this hormetic mechanism, permitting a progressive and continued hepatic injury leading to complete hepatic failure, culminating in animal death.
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PMID:Bromotrichloromethane hepatotoxicity. The role of stimulated hepatocellular regeneration in recovery: biochemical and histopathological studies in control and chlordecone pretreated male rats. 170 15

Nickel deficiency was induced in 2- to 4-year-old goats by feeding 0.1 mg Ni/kg dry matter with a semisynthetic diet. The control group consumed 5.0 mg Ni/kg d.m. Activity of several enzymes (SDH, LDH, HBDH, AST, ALT, ALD, CK, CHE) was determined in the serum, liver, heart and kidneys. Serum urea-N level was also measured and transmission electron microscopic (TEM) examinations were performed. Signs characteristic of nickel deficiency (retarded growth, increased mortality of dam and offspring, parakeratosis of the skin) appeared in the low-nickel group. The activity of SDH and ALD, as well as the level of urea-N was significantly lower in the serum of Ni-deficient animals than in the control. Ni-deficient animals also had significantly lower enzyme activities in the heart (SDH, HBDH, AST, ALT, ALD and CK), liver (SDH and CHE) and kidneys (HBDH and CK). Electron micrographs showed degeneration of cardiac and skeletal muscle in the Ni-deficient animals. Ni deficiency elicited changes primarily in the heart and these resulted in depressed activity of several enzymes.
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PMID:Effect of nickel deficiency on biochemical variables in serum, liver, heart and kidneys of goats. 178 40

To examine the combined hepatotoxic and nephrotoxic effects of cadmium and ethanol, rats maintained on an ethanol containing liquid diet (5% w/w) were given cadmium either acutely (3 x 1 mg/kg IP) or subacutely (about 14 mg/kg/day PO for 6 weeks). Parameters tested were cadmium, zinc and copper contents of blood and various organs, metallothionein (MT) contents, polysome profile of liver and kidneys, serum SDH and GPT levels and creatinine clearance. Ethanol reduced the hepatic MT contents without altering the polysome profile and the zinc and copper contents. Cadmium on the other hand raised the MT contents in liver and kidneys. This effect of cadmium predominated in the combined treatment. Morphological examination and functional tests (SDH, GPT, creatinine clearance) indicate that cadmium does not enhance the toxic effects of ethanol, and vice versa.
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PMID:Investigation into the combined effects of ethanol and cadmium on rat liver and kidneys. 227 4

The joint hepatotoxicity of CCl4 and CHCl3 or TCE in male CD rats following simultaneous oral administration has been investigated. Rats with chronic indwelling arterial cannulas were administered a single oral dose of CCl4 and CHCl3 or CCl4 and TCE in 5% Emulphor at doses of 0 to 700 mg/kg. Hepatotoxicity was evaluated by measuring the activity of AST, ALT, and SDH in plasma at 0, 3, 6, 12, 24, 36, 48, and 72 hr postgavage. Response data were analyzed for interaction using response surface methodology. CCl4 alone displayed dose-dependent toxicity. TCE demonstrated little evidence of hepatotoxicity. In combination, both CCl4/CHCl3 and CCl4/TCE displayed a synergistic (supraadditive) response for peak plasma enzyme activity.
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PMID:Interactions of water contaminants. I. Plasma enzyme activity and response surface methodology following gavage administration of CCl4 and CHCl3 or TCE singly and in combination in the rat. 234 Sep 78

The causes and clinical signs of hepatobiliary involvement in disease are many and varied and often are not referable directly to this organ system. Laboratory investigation frequently is necessary to rule hepatic disease in or out, to assess the functional impact on the liver, and to decide whether hepatic disease is the patient's primary problem or a complication of something else. The selection and interpretation of laboratory tests to resolve these problems is based on an understanding of relevant functional anatomy and pathophysiology. The mainstay of such assessment is hepatic enzymology, which can detect active disease in both hepatocytes and the biliary system. The hepatocellular pattern of disease is characterized by increases in leakage enzymes such as SDH, GLDH, and ALT and the cholestatic pattern by increases in induced enzymes (ALP and GGT). In general, enzymology does not allow the intensity or functional effect of hepatobiliary disease to be assessed, and quite severe hepatopathies may have only minimal enzyme abnormalities. For this reason, the primary biochemical data base for ruling hepatobiliary disease in or out always should involve some screening tests of hepatic function, such as albumin, protein, bilirubin, glucose, or urea determinations; as well as urinalysis to search for bilirubinuria and urobilinogenuria in hyperbilirubinemic patients and for ammonium biurate crystals when hyperammonemia or hepatic encephalopathy is suspected. Because the liver synthesizes most clotting factors, evaluation of blood coagulation is indicated when surgery is contemplated on patients with liver disease or when bleeding is present. Paired pre- and post-prandial determinations of serum bile acids are the preferred method for assessment of hepatobiliary function in dogs and cats. However, the BSP clearance test continues to be useful in the functional assessment of the liver as long as the dye remains available to veterinarians. Clearance of BSP is delayed in hepatocellular, cholestatic, and portosystemic disease as well as by severe extrahepatic circulatory disturbances, In general, this functional test is less sensitive than serum bile acids or the ammonia tolerance test in the recognition of hepatic encephalopathy caused by portosystemic anomalies. The objectives of biochemical screening of the liver are to establish the type (hepatocellular, biliary, or mixed), duration (acute, chronic), and stage (aggressive, convalescent) of hepatobiliary disease and to assess functional status.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biochemical evaluation of the hepatobiliary system in dogs and cats. 267 13

Besides hepatotoxicity, paracetamol may exert nephrotoxic effects in experimental animals and man. The present study in rats shows that cholestyramine given 4 and 24 h after paracetamol provided protection against both hepato- and nephrotoxicity; this was evidenced by reduced increments in plasma enzyme activities (SDH, GPT), indicating liver damage, and diminished retention of plasma and creatinine, indicating renal failure. The recovery of paracetamol and its conjugates in urine was markedly reduced by cholestyramine at 24-48 h after treatment. The protective effects of cholestyramine are explained by adsorption of paracetamol and conjugates in the intestine undergoing biliary excretion and enterohepatic circulation.
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PMID:Cholestyramine as an antidote against paracetamol-induced hepato- and nephrotoxicity in the rat. 274 Nov 80

In isolated, hemoglobin-free perfused livers of fasted rats, formaldehyde at an initial concentration of 10 mmol/l produced toxicity as evidenced by a release of enzymes (GPT, SDH) and of glutathione (mainly GSSG) into the perfusate, an accumulation of calcium in the liver, and a depletion of hepatic glutathione. Formaldehyde also led to an enhanced release of malondialdehyde into the perfusate, indicating peroxidative processes and decreased hepatic oxygen consumption by about 50-70%. The electron microscopic investigation of formaldehyde-exposed livers showed a destruction of the mitochondria (ruptured membranes, loss of the cristae) and some damage of the rough endoplasmic reticulum. Feeding the rats prior to surgery attenuated the hepatotoxic effects of 10 mmol/l formaldehyde. At an initial concentration of 3 mmol/l, formaldehyde did not release enzymes from livers of fed or fasted rats but only from those whose glutathione content had been depleted by treatment with phorone (250 mg/kg ip 2 h earlier). Formaldehyde liberated glucose and lactate from the livers of fed but not from those of fasted rats, indicating anaerobic energy supply in the fed state. The hepatotoxic action of formaldehyde is not due to its metabolism to formate or to the 10% methanol added as a stabilizing agent to the commercially available 37% solution named formalin. In conclusion, by destruction of mitochondria, formaldehyde inhibits aerobic energy supply and thereby presumably produces hepatocellular damage.
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PMID:Mechanistic study on formaldehyde-induced hepatotoxicity. 275 59


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