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)

Acute oral toxicity of Cd (as cadmium chloride) was enhanced in rats fasted 24 hr, as shown by a markedly decreased LD50. To examine the relationship among Cd toxicity, hepatic glutathione (GSH), and metallothionein (MT) during fasting, rats were administered 75 mg Cd/kg orally 24 hr after fasting and euthanized after a further 4 or 24 hr for various assays. Serum glutamic-pyruvic transaminase activity 24 hr after Cd treatment was higher in fasted rats than in fed rats. Both total GSH and nonprotein sulfhydryl (NPSH) concentrations in liver decreased to 50% of control levels after 28 hr of fasting and returned to 75% of control values by 48 hr. Total hepatic GSH concentration in fed rats decreased 4 and 24 hr after Cd treatment, whereas that in fasted rats remained unchanged at 4 hr and decreased significantly at 24 hr. Cd uptake by the liver (both concentration and content) 24 hr after Cd treatment was higher in fasted rats than in fed rats. Hepatic MT concentration was markedly increased by Cd treatment and higher in fasted rats than in fed rats. There was no relationship between Cd toxicity and hepatic thiobarbituric acid (TBA) value, an indicator of lipid peroxidation. Fasting had no effect on hepatic GSH peroxidase and GSH reductase activities. These enzymes probably are not involved in Cd toxicity. On histological examination, focal degenerative and necrotic changes were observed from the midlobular to the pericentral region in the livers of fed rats 24 hr after Cd treatment. These changes were enhanced by fasting, diffusing from the pericentral to the periportal region. Histochemical examination revealed a heterogeneous distribution of GSH in the livers of fed rats, with strong staining of GSH in the periportal region. This heterogeneous distribution of GSH in liver was not observed in fed rats 4 hr after Cd treatment or in fasted rats at 24 hr. The present results suggest that hepatic GSH plays an important role in protection against Cd toxicity before the onset of MT synthesis. Animals in bad condition, such as that resulting from interruption of nutrient supply, cannot be protected against Cd toxicity even if the hepatic MT level is high.
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PMID:Effects of fasting on cadmium toxicity, glutathione metabolism, and metallothionein synthesis in rats. 231 30

The activity of several blood enzymes in the presence and absence of arsenite (As) and cadmium (Cd) was investigated under in vitro conditions. Both human and rat blood glutathione peroxidase (GSH-Px) activities were adversely affected by As at the 0.8 and 1.6 micrograms/ml levels. The latter was completely inactivated whereas the former retained approximately 30% of its original activity. The effect of Cd on this enzyme was much smaller: 650 g Cd/ml were needed to decrease its activity by 30% of the original value. As noted for GSH-Px, the rat's glutamyl oxaloacetate transaminase (GOT) appears to be appreciably more sensitive to the As inhibitory effect than the human enzyme (by a factor of 3). Cd, however, failed to bring about any inhibition of GOT. In the case of glutamyl pyruvate transaminase (GPT) both As and Cd had a marked effect, manifested in 70% and 78% inhibition, respectively. Blood glucose-6-phosphate dehydrogenase (G-G-PD) was inhibited by both Cd and As, however, within the concentration range used, only Cd inhibited it completely. Cholinesterase (ChE) activity was inhibited completely by both Cd and As.
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PMID:In vitro effects of cadmium and arsenite on glutathione peroxidase, aspartate and alanine aminotransferases, cholinesterase and glucose-6-phosphate dehydrogenase activities in blood. 261 33

The study embraces the shops: metallurgic, electrolysis, production of sulfuric acid and shop 100. Tests are performed on the environmental pollution by dust, sulfur dioxide, chlorine, aerosols of sulfuric acid, carbon monoxide, nitric oxide and dioxide, hydrogen chloride, arsenic (II) oxide (III), selenium, tellurium and metal aerosols: lead, copper, cadmium and zinc. The total concentrations of chemical noxae, generating multicomponent mixtures with one-way effect on the work place, are reckon, and estimation in the Bulgarian Institute of Hygiene and Occupational Health and the Ministry of public health methods. In the same shop is comprised a representative group of workers with paraclinical tests: GOT and GPT activity, content of copper and zinc in blood. The assessment made on the work conditions and the changes already found in the workers lead to a discussion for optimizing the conditions in the new shops for copper production.
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PMID:[Hygienic evaluation and the effects of toxic factors in the work environment of copper-processing plants]. 263 3

Studies were carried out on the effect of various cadmium doses, which were given to growing rats in diet. A 42-day biological experiment was carried out on male growing Wistar rats. The animals divided into groups were given diets containing cadmium in amounts of 50, 100 and 200 ppm and diet with no adding cadmium. The diets contained 20% of protein in equal amounts from wheat gluten and casein. It was demonstrated that cadmium had a significant influence on diet intake and growth of rats. The absorption from diets containing 50, 100 and 200 ppm of cadmium was about 30 to 48%. The more cadmium was absorbed, the most was in blood and rat liver. Anaemia was noted in animals, which were given diets with cadmium. Rats had a low level of haematocrit and haemoglobin in plasma. It was shown that cadmium intake caused a significant decrease in plasma albumin concentration and increase of plasma alanine aminotransferase and aspartate aminotransferase activity.
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PMID:[Effect of various cadmium doses in the diet on the body of growing rats]. 263 83

Humans risk inadvertent intraperitoneal or intravenous exposure to formaldehyde (HCHO), commonly used for disinfection of implanted or extracorporeal medical devices. Various chemical and physical stresses are known to induce hepatic metallothionein. This study examined the effect of acute parenteral administration of HCHO on induction of hepatic metallothionein synthesis. Adult male CF1 mice were administered HCHO ip and hepatic metallothionein was quantified by the cadmium-radioassay method. HCHO (50 mg/kg) increased hepatic metallothionein as early as 8 hr after dosing with maximal levels (27-fold increase) occurring at 72 hr. Metallothionein concentrations were elevated (15-fold) 24 hr after 50 or 100 mg HCHO/kg but not at lower dosages. Concomitant elevations in hepatic zinc and copper content were observed. No increases in metallothionein were observed in kidney, pancreas, or intestine 24 hr after HCHO administration (100 mg/kg, ip). Induction of metallothionein by HCHO may reflect direct de novo synthesis since the response was abolished by pretreatment with the RNA synthesis inhibitor, actinomycin D. HCHO induction of metallothionein also does not appear to be mediated by stress-induced release of corticosteroids or catecholamines from the adrenal since the response was unaltered in adrenalectomized mice. Interference with the glutathione (GSH)-dependent oxidation of HCHO by reducing hepatic GSH concentrations to 40% of control after a 2-hr pretreatment with phorone decreased the metallothionein induction response to HCHO by 33%. This result suggests that the induction may be partially due to a HCHO metabolite, e.g., formate. Confirmation of metallothionein synthesis was obtained following spectral and chromatographic analysis. Thus, HCHO and/or a metabolite produces a marked increase in hepatic metallothionein and alters hepatic zinc and copper homeostasis, all of which are transient responses. Although HCHO was only mildly hepatotoxic at the highest dose (as evidenced by an increase in plasma alanine aminotransferase activity), such changes in metallothionein synthesis and essential metal homeostasis may be part of a cellular repair mechanism operant after acute toxic cell injury.
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PMID:Acute exposure to formaldehyde induces hepatic metallothionein synthesis in mice. 271 95

The effect of cadmium administration on female Bufo regularis was studied. The median lethal doses were 22, 18, 15 and 6.2 mg Cd2+/kg after 24, 48, 72 and 96 hr respectively. After a single intramuscular injection of 6.2 mg Cd2+/kg (representing 96-hr LD50), the results indicated that Cd2+ causes severe physiological abnormalities to this experimental animal. The serums alanine aminotransferase (AlAt), aspartate aminotransferase (AAt), alkaline phosphatase (AlP) and lactic dehydrogenase (LDH) were elevated while the calcium serum was not influenced by Cd2+ throughout the experimental period. On the other hand, phosphorus, total protein and total bilirubin were increased. EDTA treatment (0.2 mmole/kg) protected female toads from mortality up to 20 mg Cd2+/kg. It overcame the physiological alterations that were caused by the Cd2+ injection. This may be due to the fact that Cd2+ is bound to EDTA in a strong complex which is readily excreted via the kidneys.
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PMID:Toxicity of cadmium administration to the toad and the treatment of its poisoning with EDTA. 287 99

The administration of sodium N-methyl-N-dithiocarboxy-D-glucamine (NaG) at 500 mg/kg, i.p., or sodium calcium diethylenetriaminepentaacetic acid (DTPA) at 632.5 mg/kg, i.p., reduces the serum enzyme levels characteristic of hepatic damage following the intravenous administration of cadmium chloride (3.5 mg CdCl2.2.5H2O/kg). Some effect on serum enzyme levels was found even when the interval between administration of cadmium chloride and that of the antagonist was as great as 4 h. The enzymes examined included aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), alanine aminotransferase (SGPT), and alkaline phosphatase (AP). A histopathological examination of the livers of such animals also reveals the presence of a significant protective action.
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PMID:Chelating-agent suppression of cadmium-induced hepatotoxicity. 289 Jul 68

1. The effect of an acute testicotoxic dose of cadmium (CdCl2.H2O, 2.0 mg/kg i.p.) on liver morphology and drug-metabolizing enzyme activities were studied in adult male and female rats. 2. Cd treatment to female rats caused a slight and reversible decrease in hepatic microsomal aryl hydrocarbon hydroxylase (AHH) and aminopyrine N-demethylase (APND) activities. 3. No significant changes were noted in the liver morphology, serum alanine aminotransferase activities, enzyme induction by phenobarbital and 3-methylcholanthrene, and glucuronosyl-transferase (GT) and glutathione S-transferase (GST) activities. 4. The same Cd treatment to male rats, however, resulted in a much more pronounced and prolonged reduction in AHH and APND activities, which was attributable to a Cd-induced testicular necrosis and, hence, impairment of androgen secretion. 5. Accordingly, Cd treatment to castrated male rats did not lower the enzyme activities any further, and full recovery of activities was obtained after the administration of testosterone. 6. Both GT and GST, the two sex-independent enzymes, were not significantly affected by either Cd or gonadectomy in the male rat. 7. The present data show that a low acute dose of Cd induces chemical castration without severely altering hepatic function.
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PMID:Effects of a testicotoxic dose of cadmium on the liver and drug metabolism in the rat. 289 6

During a 3-month experiment is studied the effect of enriched with iron, calcium, phosphorous and vitamin D2 food ration on the changes in the organospecific enzymes in everyday introduction in the organism of experimental animals of cadmium sulfate in dose 1/40 LD50 (7 mg/kg-1). The serum activity of GOT and GPT is traced in dynamics at the end of the first, second and third month, as well as the activity of gamma-GT, LAP and APh in homogenates of liver and kidneys. The changes established in most of the experimental groups and the dates of observation show an increase in the serum and tissue activity of the examined enzymes (GOT, GPT, LAP). The tissue activity of gamma-GT and the quantity of free sulfhydryl groups are decreased in some of the dates of observation (I and III month). Both the isolated effect of cadmium and enriched food ration and their combined effect are discussed.
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PMID:[Changes in organ-specific enzymes under the influence of an enriched food ration in experimental cadmium poisoning]. 324 92

Isolated perfused livers from male and female Sprague-Dawley rats were exposed to cadmium chloride (50 and 200 microM). Acute hepatotoxicity was investigated by measuring cadmium-induced changes in bile flow, urea synthesis and alanine aminotransferase (ALT) leakage. Cadmium-induced lipid peroxidation was estimated by formation of conjugated dieners and thiobarbituric acid (TBA) reactants. Cadmium, at both concentrations, caused a rapid decrease in bile flow (within 40 min) and complete cholestasis within 70 min exposure in livers perfused from both male and female rats. Cadmium exposure (50 and 200 microM) also resulted in the leakage of ALT into the perfusate within 60 min. In contrast, exposure of isolated rat hepatocytes to as high as 500 microM cadmium did not result in enzyme leakage until 180 min exposure. Sex differences in cadmium-induced cholestasis and ALT leakage were not observed at these concentrations. Malondialdehyde was not detected in the perfusate nor were conjugated dienes detected in liver tissue following 90 min cadmium exposure. These data demonstrate that the isolated perfused rat liver (IPRL) is a sensitive system in which to study chemically induced hepatotoxicity. Cadmium rapidly causes functional alterations and cellular damage in perfused livers from both male and female rats. Cadmium-induced liver injury was apparently not related to lipid peroxidation.
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PMID:Cadmium toxicity in the isolated perfused rat liver. 378 65


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