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

Some methodological problems in clinical enzymology, including instability of enzymes in the incubation mixture and requirements for optimal reaction conditions, are highlighted. The importance of a knowledge of fundamental enzyme biochemistry and physiology as the basis for their diagnostic application is stressed, and the different behaviour of some hepatic enzymes--namely, GOT, GPT, gamma-GT, and OCT, in various pathological conditions is traced back to their characteristic biochemical and physiological properties. In the field of urinary enzymes a knowledge of the ideal requirements for the enzyme investigation of the various renal functions and of the properties of potentially valuable enzymes permits a critical selection of the really useful ones.
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PMID:A new look at the measurement and interpretation of enzyme assays. 0 46

The protective effect of pyridoxine-2-oxoglutarate (ACP) was studied on CCl4-intoxicated rats. A sensitive improvement of hepatic conditions was shown in ACP-treated rats as compared with untreated ones and rats treated with 2-oxoglutarate and pyridoxine. Serum GOT, GPT, OCT activities, composition of serum proteins, liver mitochondria respiratory control index and liver microsomes oxidizing activity were tested. The antiketotic properties of ACP were also demonstrated in Streptozotocin treated rats.
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PMID:Effect of ACP (pyridoxine-2-oxoglutarate) on CCl4 intoxication and in streptozotocin-induced ketosis in rat. 15 Jul 79

Rat serum and liver ICDH, OCT, GOT and GPT activities are significantly elevated 2-6 hr after i.p. injections of single doses (2.5 mg/kg body wt) of dichlorvos. ICDH, OCT, GOT and GPT activities are significantly increased in serum and liver of rats receiving daily injections (0.25 mg/kg body wt) for 7 days. Although liver SD is significantly elevated in the single and repeated dosage study, serum SD appears unaffected at these levels of dichlorvos toxicity. Changes in serum OCT activity estimations maybe a useful single parameter for screening pesticides for potential hepatotoxic effects in humans and farm animals.
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PMID:Serum and liver enzyme changes in rats after short term exposure to dichlorvos. 287 12

Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis (ICC), the rat shows only minimal hepatic damage on copper-loading. To investigate the possibility that copper deposition may potentiate the effects of a superimposed hepatitis, D-galactosamine (GalN) was given to copper-loaded and control rats. In the non-copper-dosed rats, GalN 0.85 g/kg i.p. produced elevated serum AST (3731 +/- 545 IU/l; normal 64.8 +/- 2.1), ALT (2090 +/- 190 IU/l; normal 18.0 +/- 0.7), and OCT (16.7 +/- 2.6 mmol/min/ml; normal 0.12 +/- 0), and liver cell necrosis with portal infiltration. In rats whose liver copper was elevated to 1298 +/- 169 micrograms/g (control 18.7 +/- 1.7) by oral copper supplementation, GalN produced much smaller increases in AST (825 +/- 122 IU/l), ALT (103 +/- 15 IU/l) and OCT (0.27 +/- 0.02 mmol/min/ml) and minimal histological damage. Viable bacterial cell counts from faecal homogenates showed that the anaerobically cultured bacteria were reduced on copper-dosing of rats. Therefore the protective effect of copper may be due to a decrease in gut-derived endotoxin acting on the liver, or to an impaired prostaglandin synthesis or perhaps to synthesis of acute phase reactants.
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PMID:Copper protects against galactosamine-induced hepatitis. 365 8

Evidence previously reported suggest that 1,3-butanediol (BD) enhances the hepatotoxic effect of a single small dose of carbon tetrachloride (CCl4) in a dose-related manner. The present study provides additional information concerning the quantitative relationship between the severity of the ketotic state produced by BD and the magnitude of the potentiation observed and emphasizes the use of ketone bodies (KB) to predict the potential hazard of the BD-CCl4 interaction. Liver damage was modulated in male Sprague-Dawley rats by varying the concentration of the BD solutions ingested prior to a CCl4 challenge (0.1 ml/kg, i.p.). These data were compared to ketone bodies in plasma, hepatic tissue and urine. BD produced a dose-dependent metabolic ketosis observable at dosages between 1.1 and 9.9 g/kg per day given for 7 days. Plasma and liver data correlated well together. Concomitantly, potentiation of the CCl4-induced liver injury was also dose-related for the same dosage range; the minimum effective dosage of BD for potentiation was estimated as 1.1 g/kg per day. The linear correlations between hepatic or plasma KB values and the indices of hepatic dysfunction (ALT, OCT) were highly significant. Using a semiquantitative method, a correlation was also found for the urinary KB data. These results suggest that plasma KB concentrations might be useful for predicting possible potentiation of the hepatonecrotic effect of CCl4 by BD.
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PMID:1,3-Butanediol-induced increases in ketone bodies and potentiation of CCl4 hepatotoxicity. 372 92

The administration of some ketonic or ketogenic compounds prior to a challenging dose of CCl4 potentiates the hepatic damage induced by this haloalkane. However, nothing is known about the recovery from the liver injury in these cases of chemically induced potentiation. To investigate this problem, we performed a temporal analysis of the hepatotoxic response of male Sprague-Dawley rats to CCl4 following a single pretreatment (p.o.) with: n-hexane, 2-hexanone, 2,5-hexanedione (15 mmol/kg in corn oil), isopropanol, acetone (33 and 34 mmol/kg in water, respectively); or the vehicle alone (10 ml/kg). They received, 18 h later, an i.p. injection of CCl4 (0.1, 0.75 or 1.0 ml/kg) and were killed 24-120 h later. Liver damage was assessed biochemically (ALT, OCT) and morphologically. A good correlation between biochemical and morphological results was observed. The ketonic or ketogenic compounds studied potentiated the liver injury produced by 0.1 ml/kg CCl4. Relative ranking orders regarding severity of maximal hepatic damage induced and time needed for complete recovery of liver injury were established; time of recovery was dependent on the maximal severity of the lesion, regardless of the potentiation. The results show that the temporal evolution of CCl4-induced liver injury is not markedly influenced by the administration of ketonic or ketogenic compounds as pretreatments, but rather depends on the severity of the maximal damage induced by the overall treatment.
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PMID:Temporal analysis of rat liver injury following potentiation of carbon tetrachloride hepatotoxicity with ketonic or ketogenic compounds. 400 41

Female Sprague-Dawley rats (175-200 g) were maintained on a commercial powdered rat chow containing 0 or 10 ppm chlordecone (Kepone; CD). On day 15 of the dietary protocol, a single dose of CCl4 (5-100 microliters/kg) was administered i.p. in corn oil vehicle. Controls received corn oil vehicle only. Twenty-four hours after CCl4 administration, hepatotoxicity was assessed using biochemical, functional, and histopathological parameters. Serum enzymes (GPT, GOT, ICD and OCT) were elevated in a dose related manner in the animals receiving CD-CCl4 combination. CCl4 alone at the doses used had no marked effect. Centrilobular necrosis was observed in the animals receiving CD-CCl4 combination. Biliary excretion of phenolphthalein glucuronide (PG) and the rate of bile flow were decreased in a dose-dependent manner. Forty-eight hour LD50 of CCl4 was decreased 26-fold by CD pretreatment. These results indicate that CD potentiates CCl4 toxicity in female rats as well. Since the hepatic functional status is greatly compromised, the CD potentiated lethality is preceded by hepatic failure. Furthermore, female rats are sensitized to smaller doses of CCl4 in comparison to male rats.
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PMID:Potentiation of CCl4 hepatotoxicity and lethality by chlordecone in female rats. 619 Feb 68

A semiquantitative morphologic procedure has been applied to chlordecone potentiation of CHCl3-induced liver injury in male Sprague-Dawley rats. The distance of the injured area from the terminal hepatic venule (THV) to the portal area was measured and the damaged cells were classified by type. The results were plotted graphically, along with elevations in plasma enzyme activities (GPT and OCT), to depict the pattern of damage. Chlordecone pretreatment enhanced the severity of the CHCl3-induced cellular changes and increased the number of cells affected. Dosages of 5 mg/kg of chlordecone did not potentiate CHCl3 toxicity, but higher dosages (10-50 mg/kg) enhanced the toxic response in a dose-dependent manner.
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PMID:A semiquantitative morphologic assessment of chlordecone-potentiated chloroform hepatotoxicity. 619 77

The propensity of chlordecone (CD) to potentiate CCl4 hepatotoxicity in rats of either sex has been well documented. The objective of the present study was to investigate the hepatotoxic effects of CD-CCl4 interaction in adrenalectomized rats. Adrenalectomized rats were maintained on 0 or 10 ppm CD and on day 15 they received a single ip injection of 25 microL CCl4/kg. Hepatotoxicity was assessed by hepatofunctional, biochemical and histopathological parameters, 24 hrs after CCl4 challenge. CCl4-induced hepatobiliary dysfunction and elevation of serum enzymes (GPT, GOT, ICD and OCT) were evident. Hepatic dysfunction was most severe in adrenalectomized rats receiving CD-CCl4 combination treatment. Histopathology of liver exhibited extensive fatty infiltration in the entire lobular structure accompanied by some necrosis. These data indicate that the capacity of CD to potentiate CCl4 hepatotoxicity is unaffected in adrenalectomized rats.
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PMID:Effect of adrenalectomy on chlordecone potentiation of carbontetrachloride hepatotoxicity. 619 34

Health conditions were evaluated in 80 electrical workers exposed for many years to polychlorinated biphenyl (PCB) mixtures with a 42% mean chlorine content, who had blood PCB concentrations from 41 to 1319 micrograms/kg. The clinical study was based on personal history data, physical examination, and laboratory tests (red cell and leukocyte count; determination of haemoglobin, packed cell volume, bilirubin, serum protein electrophoretic fractions, pseudocholinesterase, AST, ALT, GGT, and OCT). Fifteen workers were found to have skin diseases--chloracne (4), folliculitis (4), oil dermatitis (1), juvenile acne (1), and dermatitis due to irritative or allergic agents (5). Sixteen workers showed more or less pronounced hepatic involvement, consisting most often of hepatomegaly with an increase in serum GGT, AST, ALT, and OCT values. In two workers bleeding cavernous haemangiomas were discovered, in one case associated with chronic myelocytic leukaemia. All the workers with chloracne were employed on electric capacitor impregnation with PCBs, and no definite association was found between chloracne and blood PCB concentrations. Conversely, a significant positive association was found between the abnormal liver findings and blood PCB concentrations, particularly trichlorobiphenyl blood concentrations. The abnormal hepatic findings observed are similar to those reported in experimental animals given PCBs, and in some workers such findings should probably be considered as clinical signs of hepatic microsomal enzyme induction.
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PMID:Occupational exposure to polychlorinated biphenyls in electrical workers. II. Health effects. 645 Dec 37


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