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)

A Pacific white-sided dolphin (Lagenorhynchus obliquidens) developed clinical signs, serum biochemical values, and serologic viral markers consistent with chronic persistent hepatitis caused by a hepatitis B-like virus. The hepatitis had a sporadic cyclical pattern of lethargy, inappetance, and icterus, with leukocytosis and increased serum activities of alanine transaminase, aspartate transaminase, and gamma-glutamyltransferase. The serum from this dolphin contained hepatitis B virus core antibodies, hepatitis B surface antibodies, and hepatitis B viral DNA. Supportive treatment consisted of administration of antibiotics, cimetidine, menadiol sodium diphosphate, and vitamin/dextrose supplementation. A clinically normal killer whale (Orcinus orca) housed in the same pool had serum hepatitis B surface antibodies, suggesting immunologic responsiveness and that this disease was not species-specific.
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PMID:Hepatitis B-like infection in a Pacific white-sided dolphin (Lagenorhynchus obliquidens). 229 47

Clinical studies of imipenem/cilastatin sodium (IPM/CS) were conducted in 40 pediatric patients. 29 out of the 40 patients were treated for infections and 11 for prophylaxis. The following results were obtained. 1. The response rate in 29 patients with infections was 79.3%. Among the 29 patients, 16 patients who presented with malignant diseases showed the response rate of 68.8%. The response rate was lower in patients with severe infections than in those with mild or moderate infections, and a lower response rate was associated with severe neutropenia. However, there were no differences in the response rates between patients who had previously been treated and those who had been untreated with other antibiotics. The response rate in 6 patients from whom causative organisms were isolated was 83.3% and that in the remaining 23 patients was 78.3%. 2. The response rate in 11 patients to whom IPM/CS was administered prophylactically was 63.6%. 3. As for side effects, a rash was observed in 1 patient and hematuria in another, and the abnormal laboratory test results observed were elevations of GOT and GPT in 1 patient. However, they were not clinically significant. From the above results, it appears that IPM/CS may be used as a drug of the first choice for the treatment of patients with severe infections in which the causative organisms are unknown, and for the prophylaxis of infection in patients with neutropenia.
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PMID:[Clinical study of imipenem/cilastatin sodium in children with severe infections]. 234 51

The hepatotoxicity of acetaminophen is believed to be mediated by the metabolic activation of acetaminophen to N-acetyl-p-benzoquinone imine which covalently binds to cysteinyl residues on proteins as 3-(cystein-S-yl)acetaminophen adducts. The formation of these adducts in hepatic protein correlates with the hepatotoxicity. In this study, the formation of 3-(cystein-S-yl)acetaminophen adducts in specific cellular proteins was investigated using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and detected using affinity-purified antisera specific for 3-(cystein-S-yl)acetaminophen adducts on immunoblots. These techniques were used to investigate the liver 10,000g supernatant and serum from B6C3F1 mice that received hepatotoxic doses of acetaminophen. More than 15 proteins containing 3-(cystein-S-yl)acetaminophen adducts were detected in the liver 10,000g supernatant. The most prominent protein containing 3-(cystein-S-yl)acetaminophen adducts in the hepatic 10,000g supernatant had a relative molecular mass of 55 kDa. Serum proteins containing 3-(cystein-S-yl)acetaminophen adducts had molecular masses similar to those found in the liver 10,000g supernatant (55, 87, and approximately 102 kDa). These data, combined with our previous findings describing the temporal relationship between the appearance of 3-(cystein-S-yl)acetaminophen adducts in protein in the serum and the decrease in the levels of 3-(cystein-S-yl)acetaminophen adducts in protein in the liver, suggested that liver adducts were released into the serum following lysis of hepatocytes. The temporal relationship between the formation of specific adducts and hepatotoxicity in mice following a hepatotoxic dose of acetaminophen was examined using immunoblots of mitochondria, microsomes, cytosol, and plasma membranes. Hepatotoxicity indicated by serum alanine aminotransferase levels was increased at 2 and 4 hr after dosing. The cytosolic fraction contained numerous proteins with 3-(cystein-S-yl)acetaminophen adducts, the most intensely stained of which was a 55-kDa protein. 3-(Cystein-S-yl)acetaminophen adducts were detected in the 55-kDa liver protein 30 min after dosing and prior to the development of significant toxicity. Examination of gels suggested that maximal levels of immunochemically detectable adducts in the 55-kDa protein occurred at 1-2 hr, with a decrease in intensity 4 hr after dosing. The presence of 3-(cystein-S-yl)acetaminophen adducts in proteins prior to hepatotoxicity suggests a threshold for adduct formation in the development of toxicity. Protein in microsomes which contained 3-(cystein-S-yl)acetaminophen adducts ranged in molecular weight from 38 to approximately 106 kDa. The major proteins containing 3-(cystein-S-yl)acetaminophen adducts in the mitochondria had molecular masses of 39, 50, 68, and 79 kDa.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunoblot analysis of protein containing 3-(cystein-S-yl)acetaminophen adducts in serum and subcellular liver fractions from acetaminophen-treated mice. 238 41

The status of Na+ regulation was examined during early stages of alkylation insult to rat liver. Na+/K+-ATPase activity in plasma membranes declined by 52% within 3 hr of treatment with 850 mg/kg acetaminophen. This loss preceded the release of alanine aminotransferase (2880 +/- 1550 U/ml) and necrosis (2+) seen at 24 hr. Activities of 5'-nucleotidase and Mg2+-ATPase and recovery of plasma membranes were comparatively unchanged at 3 hr. Because damage to Na+/K+-ATPase appeared early in the pathogenesis of acetaminophen hepatotoxicity, loss of hepatocellular Na+ regulation could represent one of the critical molecular consequences of lethal alkylation by acetaminophen.
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PMID:Early inhibition of the Na+/K+-ATPase ion pump during acetaminophen-induced hepatotoxicity in rat. 244 17

The propensity of chlordecone (CD) to potentiate hepatotoxic and lethal effects of CCl4 is well established. Mirex (M), a close structural analogue of CD, or phenobarbital (PB), powerful inducers of hepatic microsomal drug metabolizing enzymes, are much weaker potentiators of CCl4 toxicity. The purpose of this study was to test the possibility that CD potentiates the toxicity of CCl4 by increasing the metabolism of CCl4 to a greater degree than either PB or M. We compared the in vivo metabolism of CCl4 in rats pretreated with CD, M, or PB, by measuring the hepatic content of 14CCl4, the expiration of 14CCl4, expiration of 14CCl4-derived 14CO2, and lipid peroxidation. Male Sprague-Dawley rats (250-270 g) were pretreated with a single oral dose of CD (10 mg/kg), M (10 mg/kg), or corn oil vehicle (1 ml/kg). PB pretreatment consisted of an ip injection of sodium PB (80 mg/kg) in saline (0.9%) for 2 successive days. Twenty-four hours later, 14CCl4 (0.1 ml/kg; sp act: 0.04 mCi/mmol) was administered ip in corn oil and the radioactivity present in the expired air was collected for 6 hr. Excretion of the parent compound as represented by the 14C label in the toluene trap was unchanged by any of the pretreatments. Expiration of 14CO2 measured during the 6 hr after CCl4 administration was increased in animals pretreated with PB or CD. In vivo lipid peroxidation measured as diene conjugation in lipids extracted from the livers was increased to a similar extent in animals pretreated with PB and CD, whereas the serum transaminases (ALT, AST) were significantly elevated only in animals pretreated with CD.M did not affect 14CO2 production and was without a significant effect on the lipid peroxidation. The radiolabel present in the liver at 6 hr showed no difference in hepatic content of free 14CCl4 among the groups, but the covalently bound label present in the lipid fractions of the livers pretreated with PB was elevated in comparison to CD and M treatments. These data indicate that a single oral administration of CD (10 mg/kg) 24 hr prior to CCl4 administration (100 microliter/kg) enhances the oxidative metabolism of CCl4 but to a lesser extent than PB (80 mg/kg, ip, twice), which is in inverse relationship to the potentiation of the hepatotoxic and lethal effects of CCl4 associated with these pretreatments.
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PMID:In vivo metabolism of CCl4 by rats pretreated with chlordecone, mirex, or phenobarbital. 245 66

The authors studied the pharmacotherapeutic efficacy of antioxidants vitamin E, sodium selenite, and their combination in damage to rat liver by CCl4 and the anthelmintic agent chloxyl. Changes of the intensity of peroxidation of biological membrane lipids, the activity of enzymes-markers of hepatocyte cytolysis--alanine aminotransferase and aspartate aminotransferase--in blood serum, and changes in the structure of the liver were studied. Antioxidants and their combination blocked lipid peroxidation, reduced the activity of alanine aminotransferase and aspartate aminotransferase in blood serum considerably, and caused a protective effect on the structure of rat liver in its damage by CCl4 and chloxyl.
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PMID:[Experimental antioxidant therapy in toxic liver damage from CCl4 and chloxyl]. 255 82

The liver and kidney tolerance of iopromide 370 in comparison to that of sodium meglumine diatrizoate 370 or iopamidol 370 in doses of 2 ml/kg body weight was examined in two controlled double-blind studies with intravenous digital subtraction angiography on the basis of enzyme assays in serum and urine. In patients with normal kidney function no changes were observed in the levels of the liver enzymes GPT, GOT, and gamma glutamyl transpeptidase (GGT) serum up to 72 hours after injection of iopromide or sodium meglumine diatrizoate. Among the kidney-specific enzymes, the excretion of GGT in urine increased after injection of iopromide and iopamidol. The maximum increase of GGT excretion was, however, statistically significantly lower in the group treated with iopromide than in the iopamidol group. Within 72 hours, the activities had been returned to the initial values in both groups.
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PMID:Renal and hepatic tolerance of nonionic and ionic contrast media in intravenous digital subtraction angiography. 256 17

Adult female rats were orally dosed with 1/5 to 3/5 the published LD50 of either promoters or putative promoters of carcinogenesis [hexachlorobenzene (HCB), alpha-hexachlorocyclohexane (alpha-HCH), kepone and toxaphene] or noncarcinogens [coumaphos, EDTA, caprolactam, 8-hydroxyquinoline, titanium (IV) oxide, sodium diethyldithiocarbamate (DEDTC), and sucrose] at 21 and 4 h before sacrifice. The promoters selected in this study were all of the halogenated hydrocarbon class. At doses of 1/5 to 3/5 the LD50, all four promoters or putative promoters induced rat hepatic ODC activity. The seven noncarcinogens produced several biochemical effects at doses of 1/5 the LD50: increased serum alanine aminotransferase activity (SGPT) (caprolactam and DEDTC), decreased hepatic cytochrome P-450 content (DEDTC), and increased hepatic ODC activity (8-hydroxyquinoline and DEDTC). None of the seven noncarcinogens caused hepatic DNA damage or coordinate induction of hepatic ODC and cytochrome P-450. The results support the interpretation that several of these biochemical parameters are useful in distinguishing potential tumor promoters and noncarcinogens.
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PMID:Biochemical studies of promoters of carcinogenesis in rat liver. 257 89

Serum osmolalities and osmolar gap were determined in 43 normal healthy beagles (control group) and 40 dogs with dirofilarial hemoglobinuria (hemoglobinuria group). In the control group, the measured and calculated serum osmolality levels were in the means of 296 +/- 5 (SD) mOsm/kg and 293 +/- 6 mOsm/kg respectively, showing an osmolar gap less than 10 mOsm/kg. In the hemoglobinuria group, the measured serum osmolality ranged from 272 to 370 mOsm/kg. A considerable number of dogs had normal serum osmolalities in spite of severe intravascular hemolysis, suggesting that the changes in serum osmolality would not be the direct cause of intravascular hemolysis. The measured serum osmolality (331 +/- 28 mOsm/kg) was significantly higher in 11 dogs which died after a surgical removal heartworms than in 29 dogs which recovered after the removal (302 +/- 17 mOsm/kg). The calculated serum osmolality level was 296 +/- 16 mOsm/kg in 24 recovered cases, and 304 +/- 22 mOsm/kg in 10 fatal cases. The osmolar gap stayed in the normal ranges of 5.4 +/- 5.9 mOsm/kg in recovered cases, but it attained a higher level of 22.7 +/- 8.9 mOsm/kg in fatal cases, suggesting poor prognosis in cases with large osmolar gaps. There were significant positive correlations between the measured serum osmolality and osmolar gap, serum sodium, potassium, BUN, GOT, GPT, creatinine, bilirubin and plasma hemoglobin values, as well as between the osmolar gap and serum potassium, BUN, GOT, GPT, creatinine and bilirubin values. The plasma hemoglobin concentration fell markedly without significant change in serum osmolality 20 hr after the heartworm removal.
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PMID:Clinical studies on canine dirofilarial hemoglobinuria: measured and calculated serum osmolalities and osmolar gap. 258 25

Thirty female beagle dogs, 7 to 8 months old, were assigned to five groups. Control, low dosage, medium dosage, high dosage, and pair-fed groups were offered 0, 1, 2, 4 and 0 mg of sodium arsenite per killigram of body weight per day (mg/kg/day), respectively, in their feed. On Day 59, the dosage was doubled for the rest of the experiment, which ended on Day 183. Nominal dosages of 4 and 8 mg/kg/day caused a significant decrease in feed consumption. The initial decreased feed consumption was followed by increased intake over time. Nominal dosages of 4 and 8 mg/kg/day caused a significant decrease in body weight. Body weight loss of high dosage and pair fed groups were not significantly different. Serum aspartate aminotransferase was elevated in dogs exposed to 4 and 8 mg/kg/day of sodium arsenite. Serum alanine aminotransferase was elevated in dogs exposed to 2, 4, and 8 mg/kg/day. No gross or light microscopic lesions were present in the liver of any group. This study shows that dietary sodium arsenite causes a dose-dependent decrease of feed consumption and body weight. Weight loss is caused by decreased feed consumption, not by the direct effect of the sodium arsenite.
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PMID:Effect of subacute low level dietary sodium arsenite on dogs. 261 77


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