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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For 70 days two groups of 10-week gilts were given feed supplemented with PCB commercial mixture of Czechoslovak make (Delor 105), at the doses of 10 and 50 mg. .kg-1 of feed. Over the experimental period, animals were administered 1000 mg or 5000 mg of PCB mixture. During the experimental period the levels of glucose, cholesterol, urea, total protein, vitamin A, calcium, inorganic phosphorus and the activities of AF, ALT and AST enzymes were determined twice. At the end of this experiment the aniline hydroxylase activity in microsomal fractions of liver was determined and pronounced induction effect of PCB on the enzymatic system was observed. Out of the studied metabolic parameters of blood plasma, the decrease in vitamin A level was significant.
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PMID:[The effect of polychlorinated biphenyls (PCB) on liver aniline hydroxylase activity and on certain metabolic parameters in the blood of pigs]. 642 Sep 73

Acute or chronic treatment of rats with isopropanol caused a significant increase in hepatic cytochrome P-450 content and a two- to threefold increase in aniline hydroxylase and 7-ethoxycoumarin O-deethylase activities, but no significant change in ethylmorphine N-demethylase or benzo(a)pyrene hydroxylase activity. In rats treated with isopropanol and challenged with CCl4, liver toxicity of CCl4 was characteristically potentiated, as assessed by elevation of serum glutamic-pyruvic transaminase (SGPT) levels. Isopropanol pretreatment also potentiated CCl4-induced damage to the hepatic monooxygenase system. In addition to a decrease in cytochrome P-450, rats treated with isopropanol and challenged with CCl4 showed a nonspecific decrease not only in aniline hydroxylase and 7-ethoxycoumarin O-deethylase activities, but also in ethylmorphine N-demethylase, benzo(a)pyrene hydroxylase, and NADPH-cytochrome c reductase activities. These results were confirmed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of solubilized microsomes. The electrophoretic results showed that isopropanol pretreatment markedly potentiated the CCl4-caused destruction of cytochrome P-450 hemeproteins. The data strongly suggest that isopropanol increases one or more forms of cytochrome P-450 which selectively enhance the metabolism of CCl4 to an active metabolite. This active metabolite then causes a nonselective damage to the microsomal mixed-function oxidase system.
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PMID:Isopropanol enhancement of cytochrome P-450-dependent monooxygenase activities and its effects on carbon tetrachloride intoxication. 663 85

Hepatotoxicity of aflatoxin B1 (2.0 and 4.0 mg/kg i.p.) as determined by plasma enzyme activities (GPT and GOT), liver triglycerides and histopathologic changes was enhanced in rats pretreated with four oral doses of ethanol (4.0 g/kg each) at 48, 45, 24 and 21 hrs prior to aflatoxin B1 administration. Pretreatment with ethanol (4.0 g/kg) slightly increased liver weight without changing hepatic microsomal protein contents. Also it caused an increase in microsomal aniline hydroxylase but a decrease in p-nitroanisole-o-demethylase, 48 hrs after the first ethanol dose. In the rats pretreated with ethanol, aflatoxin B1 was metabolized at a higher extent to aflatoxins M1 and Q1. These results suggest that an increased hepatotoxicity of aflatoxin B1 after pretreatment with ethanol may presumably due to an increase in microsomal formation of active aflatoxin B1 metabolite.
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PMID:Enhanced hepatotoxicity of aflatoxin B1 by pretreatment of rats with ethanol. 681 83

Since it is known that the metabolism of acetaminophen is involved in its hepatotoxicity and that drug metabolizing enzyme activity is decreased in tumor bearing animals, it was of interest to study the influence of L-1210 leukaemia on acetaminophen hepatotoxicity in BDF-1 male mice. A single oral dose of acetaminophen, 125 mg/kg, was given at the fifth day of the mice survival period (7.7 days) and the animals killed twenty-four hours later. As revealed by serum glutamic-pyruvic transaminase, serum glutamic-oxaloacetic transaminase and lactic dehydrogenase, acetaminophen was less hepatotoxic in leukaemic mice than in control mice by comparison with their own saline group; on the other hand the difference between control and leukaemic mice treated with acetaminophen was significant only for glutamic-pyruvic transaminase. Moreover, we found higher unchanged acetaminophen concentrations in plasma, liver, kidneys, brain and fat of the leukaemic mice as compared to controls, less conjugated metabolites in plasma and liver, decreased in vitro aniline hydroxylation and ethylmorphine N-demethylation. Finally, following acetaminophen administration, reduced hepatic glutathione was depleted to a much lesser extent in the tumor bearing animals than in controls. In conclusion, the L-1210 leukaemia seems to modify the acetaminophen hepatotoxicity and this effect might be explained by decreased acetaminophen biotransformation into toxic metabolites or intermediates.
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PMID:Influence of leukaemia on acetaminophen-induced hepatotoxicity in mice. 689 Feb 27

During the course of testing chronic toxicity in rats several physiological and biochemical parameters were investigated. Many of the processes studied show a circadian and infradian rhythm, which can clearly be influenced from the second year onwards by age dependent alterations. The daily rhythm of the following processes were investigated: Hexobarbital sleeping time, aminophenazone demethylation, Hb (Hemoglobin), Hc (Hematocrit), GPT (Glutamate-pyruvate-transaminase) and total plasma proteins. The seasonal changes of total plasma proteins, Hexobarbital sleeping time and aniline hydroxylation were also examined. The results obtained indicate, that for comparison and interpretation of data on acute and chronic toxicity the knowledge of daily and seasonal changes is necessary and has to be considered for an exact planning of experiments.
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PMID:Planning of experiments for the testing of chronic toxicity in rats taking into account biorhythms. 693 52

To find out the biochemical mechanisms involved in the hepatotoxicity of certain drugs, the continuous evolution of some related biochemical parameters was investigated. The results obtained showed the decrease of cytochrome P450, glutathione (GSH) and aniline hydroxylase, as well as increases of lipid peroxides and tryptophan oxygenase 2 hours after i.p. administration of carbon tetrachloride (CCl4) and paracetamol. Characteristic changes of hepatotoxicity such as increase of blood glutamate-pyruvate transaminase (GPT) and triglycerides, and decrease of free sulfhydryl (SH) groups were observed 24 hours after drug administration. The peroxidation of microsomal lipids appears to be the biochemical mechanism involved in the acute administration of these drugs. Subsequently this peroxidation leads to morphologic hepatic changes. In our experimental conditions, hepatotoxicity was prevented by concomitant administration of cystamine.
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PMID:Biochemical mechanisms involved in the hepatotoxicity of some drugs. 698 92

In rats, i.v. administration of praseodymium, cerium and lanthanum (3 to 14 mg/kg) produced a dose-dependent increase in the serum activities of GOT, GPT and SDH. These dose-response curves of serum enzyme activities were shifted to the right by simultaneous treatment with silybin (75 mg/kg i.p.). Silybin also attenuated the increase of bromosulphthaleine retention and prevented the accumulation of liver triglycerides induced by praseodymium (7 mg/kg i.v.). Furthermore, silybin reduced the mortality rate of rats treated with high doses of the lanthanides. Rats treated with praseodymium (7 mg/kg i.v.) developed a pronounced hypoglycemia. On the 3rd day after praseodymium injection liver glycogen decreased to 4%, liver glutathione (GSH) to 82%, hepatic microsomal cytochrome P-450 content to 53%, aniline hydroxylase activity to 58% and aminophenazone demethylase activity to 40% of the control values. Silybin prevented praseodymium-induced hypoglycemia completely and the changes in the biochemical parameters of liver function partially but did not influence the decrease of liver GSH.
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PMID:The influence of silybin on the hepatotoxic and hypoglycemic effects of praseodymium and other lanthanides. 719 8

Groups of CFY rats were exposed to toluene inhalation as follows: both males and females to 1000 mg/m3 6 h daily five times a week for 6 months; only males to 3500 mg/h3 8 h daily every day for 6 months; and only males to 1500, 3000 and 6000 mg/m3 8 h daily for 4 weeks. Control groups were exposed to air inhalation under identical conditions. Toluene was found to inhibit growth but to cause no abnormal light-microscopical changes. Hepatic changes were: (i) Signs of compensation such as increased relative liver weight, SER proliferation; increased succinate dehydrogenase activity; a decrease in glycogen content; increased cytochrome P-450 and b5 concentration; increased hepatic aniline hydroxylase and aminopyrine N-demethylase activity. (ii) Non-specific subcellular effect was observed in a small number of hepatocytes, namely RER dilatation, separation of ribosomes, mitochondria of variable shapes, an increased number of autophagous bodies. As regards indicators of the hepatic function, BSP retention decreased, GOT and GPT activity did not change. The changes were observed in both sexes, were dose-dependent and reversible, and showed no--or only a slight--dependence on exposure time. Chronic toluene exposure has no specific hepatotoxic effect leading to chronic liver disease.
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PMID:Effect of toluene inhalation on the liver of rats--dependence on sex dose and exposure time. 744 Sep 61

The purpose of this study was to investigate the role of hydrolysis products of linoleic acid anilide (LAA), i.e., aniline and linoleic acid (LA), in the toxicity to the hemopoietic system, especially to the spleen. To achieve this, the parent compound (LAA) and its putative hydrolysis products, i.e., aniline or linoleic acid (LA), were given to male SD rats at equimolar doses (0.7 mmol/kg) in 0.25 ml mineral oil by gavage, daily, for 14 days. The controls received equal volumes of vehicle only. Five animals from each group were euthanized at Days 1, 7, and 28 following the last dose. At all time points, spleen weights increased in the LAA- and aniline-treated rats, but spleen to body weight ratios were increased only at Days 1 and 7 in these groups. No changes were observed in the LA-treated rats at any time point. RBC counts were decreased in the LAA and aniline groups at Days 1 and 7, whereas hemoglobin content was decreased by 20 and 13% in the LAA- and aniline-treated rats, respectively, only at Day 1. Methemoglobin content in the LAA and aniline groups also increased by 76 and 101%, respectively, at Day 1. Serum transaminases (AST and ALT) decreased in the LAA, aniline, and LA groups but the decreases were more consistent in the LA group. Serum IgA increased in the LAA and aniline groups only at Day 1. Splenic iron content was increased 381, 486, and 51% in the LAA-treated rats and 474, 491, and 58% in the aniline-treated rats at Days 1, 7, and 28, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hematopoietic toxicity of linoleic acid anilide: importance of aniline. 766 6

Haloanilines are commonly used as chemical intermediates in the manufacture of a wide range of products. The purpose of this study was to examine the in vivo nephrotoxic and hepatotoxic potentials of the 3-haloanilines. The in vitro effects of the 3-haloanilines on renal function were also examined. In the in vivo experiments, male Fischer 344 rats (four rats/group) were administered a single intraperitoneal (i.p.) injection of an aniline hydrochloride (1.0 or 1.25 mmol kg-1) or vehicle. Renal and hepatic function were monitored at 24 and/or 48 h post-treatment. None of the 3-haloanilines were potent nephrotoxicants at either dose level. The greatest effects on renal function were observed following administration of 3-chloroaniline at a dose of 1.25 mmol kg-1 (oliguria, glucosuria, hematuria, decreased p-aminohippurate accumulation by renal cortical slices and increased blood urea nitrogen concentration). 3-Chloroaniline also was the only aniline compound to increase plasma ALT/GPT activity at 48 h. In the in vitro experiments, the ability of an aniline (10(-5) - 10(-3) M) to decrease organic ion accumulation in renal cortical slices from untreated rats was examined. The decreasing order of in vitro nephrotoxic potential was 3-iodoaniline > 3-bromoaniline > 3-chloroaniline > aniline > 3-fluoroaniline. These results indicate that the 3-haloanilines are not potent nephrotoxicants or hepatotoxicants at sublethal doses. In addition, the reasons why the 3-haloanilines have different orders of nephrotoxic potential in vivo and in vitro are not clear at this time.
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PMID:Acute renal and hepatic effects induced by 3-haloanilines in the Fischer 344 rat. 778 60


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