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)

Clinical pattern and dynamics of some biochemical indicators were observed in six four-year lambing ewes of the Improved Wallachian breed in the course of 32-day administration of magnesite fly ash. A daily dose of the tested fly ash with the content of 305,000 mg/kg magnesium amounted to 500 mg/kg live weight of sheep. The intake of concentrate mixture with magnesium content in the test sheep decreased by a third between the 12th and 20th day, by another half between the 20th and 26th day and the intake was minimum to nil during the last seven days of the trial. The decrease in the intake of concentrate mixture was accompanied by increased water consumption and by gradual inappetence for hay. Shaped droppings started to change their consistency to slurry consistency from the 12th day of observation. Thinner to watery consistency of excrements appeared in all sheep between the 15th and 20th day and diarrheas persisted in all animals until the end of the trial. The indicators of hematological profile did not show an undoubted relationship to the administration of tested magnesium, and the variations in the particular indicators observed during the trial were within the physiological range. Serum enzymes showed a significant increase against the starting values only in the concentration of alanine aminotransferase on day 20 and day 26 (p < 0.05 and/or p < 0.001). An increase in the proteosynthetic activity of hepatocytes signalled a statistically significant increase in total proteins (p < 0.05), total immunoglobulins (p < 0.05) and an insignificant increase in albumin content. Out of the analyzed mineral elements, magnesium content showed the most significant relationship to administration of industrial pollutants as its significant increase in blood serum, urine and droppings was observable since day 20 (p < 0.05, p < 0.01 and p < 0.001, respectively). The dynamics of calcium, phosphorus, potassium, sodium, iron, copper, zinc, molybdenum, arsenic and cadmium concentrations showed different patterns in the blood serum, droppings and urine of sheep in the course of magnesite fly ash feeding, and the evaluation of interactions with magnesium requires further studies.
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PMID:[Dynamics of clinico-biochemical changes in sheep during magnesite loading]. 897 53

Two gold compounds, gold sodium thiomalate (AuTM) and auranofin, are presently in clinical use in therapy of rheumatoid arthritis. In these studies, AuTM administered to Sprague-Dawley rats and three strains of mice, Swiss-Webster, C3H/HeJ, and DBA/2J, were studied with regard to its effect on liver and renal monooxygenases, metallothionein contents, and serum levels of alanine aminotransferase and urea nitrogen. These effects of AuTM were compared to those of cadmium, since the latter metal has exhibited tissue and species differences in the induction of metallothionein. Benzo(a)pyrene hydroxylase and benzphetamine N-demethylase activities were not altered by AuTM in livers of rats and the three strains of mice. Benzo(a)pyrene hydroxylase activity was significantly decreased in rat kidney, whereas this enzyme activity was not affected in the kidneys of mice. In rats, AuTM caused a sevenfold induction in liver metallothionein, while in mice, liver metallothionein was induced twofold in Swiss-Webster mice and about fivefold in the inbred strains. AuTM caused minimal changes in renal metallothionein contents in the three strains of mice studied. Serum alanine amino-transferase, an indicator of hepatotoxicity, was not altered by AuTM in rats and mice studied. Blood urea nitrogen, an indicator of kidney dysfunction, was increased threefold in rats, but not in AuTM-treated mice. These data demonstrate that AuTM, a nephrotoxic agent in rats and humans, showed no nephrotoxic effects in the mouse strains studied here.
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PMID:Species differences in the renal toxicity of the antiarthritic drug, gold sodium thiomalate. 906 47

Exposure of humans to toxic metals and metalloids is a major environmental problem. Many metals, such as cadmium, can be hepatotoxic. However, the mechanisms by which metals cause acute hepatic injury are in many cases unknown. Previous reports suggest a major role for inflammation in acute cadmium induced hepatotoxicity. In initial experiments we found that a non-hepatotoxic dose of cadmium chloride (CdCl2; 2.0 mg/kg, i.v.) markedly increased the clearance rate of colloidal carbon from the blood, which is indicative of enhanced phagocytic activity by Kupffer cells (resident hepatic macrophages). Thus. the objective these studies was to determine the involvement of Kupffer cells in cadmium induced liver injury by inhibiting their function with gadolinium chloride (GdCl3). Male Sprague-Dawley rats were administered GdCl3 (10 mg/kg, i.v.) followed 24 h later by a single dose of CdCl2 (3.0 and 4.0 mg/kg, i.v.). Twenty four hours after CdCl2 administration animals were killed and the degree of liver toxicity was assessed using plasma alanine aminotransferase (ALT), as well as light microscopy. Cadmium chloride administration produced multifocal hepatocellular necrosis and increased plasma ALT activity. Pretreatment with GdCl3 significantly reduced both the morphological changes and hepatic ALT release caused by CdCl2. However, the protection was specific to the liver, and did not alter CdCl2 induced testicular injury, as determined by histopathological damage. In many cases, the inducible cadmium-binding protein, metallothionein (MT) is often an essential aspect of the acquisition of cadmium tolerance in the liver. Although cadmium caused a dramatic induction of hepatic MT (32-fold), GdCl3 caused only a minor increase (2-fold). Combined CdCl2 and GdCl3 treatment did not induce levels to an extent greater than CdCl2 alone. As expected, GdCl3 also caused a slight increase in the amount of cadmium associated with the liver. In cultured hepatocytes isolated from GdCl3 pretreated rats, CdCl2 induced cytotoxicity was not significantly altered compared to control hepatocytes, indicating that the mechanism of tolerance required the presence of other cell types. Thus, GdCl3 attenuation of CdCl2 induced hepatotoxicity does not appear to be caused by increased tissue MT content or a decreased susceptibility of hepatocytes to cadmium. From these data, we concluded that tolerance to cadmium induced hepatotoxicity involves the inhibition of Kupffer cell function which results in a decreased inflammatory response and an altered progression of hepatic injury. These data further indicate that Kupffer cell function is critical to cadmium induced hepatocellular necrosis.
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PMID:Suppression of Kupffer cell function prevents cadmium induced hepatocellular necrosis in the male Sprague-Dawley rat. 923 Apr 47

Apoptosis is a process of active cell death, distinct from necrosis and characterized by specific morphological and biochemical features. Although the acute hepatotoxic effects of cadmium (Cd) are well described, little is known about the occurrence of apoptosis in Cd toxicity. Therefore, mice were injected with 5-60 mumol/kg i.p. of Cd and their livers were removed 1.5-48 h later and examined by light microscopy. Cd induced both a time- and dose-dependent increase in apoptotic index, severity of necrosis, and mitotic index. Apoptotic index peaked at 9-14 h after Cd administration and then decreased. The time course of apoptotic DNA fragmentation index, monitored by quantification of oligonucleosomal DNA fragments, correlated with the results obtained by histopathological analysis and a commercial in situ apoptotic DNA detection kit. Liver necrosis, as demonstrated by histology and serum alanine aminotransferase and sorbitol dehydrogenase assays, was most severe 14-48 h after Cd injection. Apoptosis was decreasing by 24 h while necrosis persisted. Replacement of liver tissue by blood lakes (peliosis hepatis) was observed after 14 h. The mitotic index increased gradually with time, indicating compensatory liver cell regeneration. There was a progressive increase in the severity of necrosis, apoptotic index, and mitotic index with increasing dose of Cd. These data demonstrate that apoptosis is a major mode of elimination of critically damaged cells in acute Cd hepatotoxicity in the mouse, and it precedes necrosis.
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PMID:Cadmium-induced apoptosis in mouse liver. 957 89

Manzala Lake exposed to many pollutants including untreated sewage, agricultural and industrial wastes which increase the concentration of heavy metals, and compromise the health state of the fishermen. This study investigated 100 fishermen and 100 males of other occupations as controls. Both groups work in and live on and around the lake. Clinical examination revealed no significant changes between the fishermen and control group as regards the cardiovascular, gastrointestinal and dermatological systems. However, the urinary, musculoskeletal and respiratory symptoms were significantly higher in fishermen than in control males. There was a significant decrease in neutrophils (48.8%) and a significant increase in lymphocytes and eosinophils (35.4% and 9%), respectively. Hepatotoxicity was evidenced by an increase in serum aspartate transaminase and alanine transaminase. There were no significant differences in serum creatinine and urea between fishermen and control. Levels of lead, cadmium and mercury in water and sediment were 0.26, 0.014, 0.002 mg/l, and 33.5, 1.37, 0.28 micrograms/kg, respectively. Levels of the three heavy metals in the fish samples and serum of fishermen and control males in average were 1.06, 0.18, 0.00025 ppm, 523, 33.5, 13.7 micrograms/l and 374, 12.8 11.2 micrograms/l, respectively. This study aimed to establish the relation between the environmental pollution and the health status of the population inhabiting the contaminated areas.
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PMID:Relationship between environmental pollution in Manzala Lake and health profile of fishermen. 958 78

The hepatotoxicity of cadmium was studied in 1-, 2-, and 6-month-old male Wistar rats. Liver damage, indicated by the increase in serum alanine aminotransferase activity 24 h after sc administration of 3 and 6 mg/kg cadmium, was observed only in 6-month-old rats. Dose-dependent increases in the cadmium content of the liver were similar for all three age groups. Basal and induced metallothionein contents were higher in livers of 1-month-old rats than in those of 2- and 6-month-old rats. In contrast, the basal glutathione content of the liver was higher in 6-month-old rats than in 1- and 2-month-old rats, and glutathione content increased slightly in all three age groups after cadmium administration. Thus, the higher susceptibility to cadmium-induced hepatotoxicity in 6-month-old rats seemed not to be explained by differences in cadmium uptake or by the metallothionein and glutathione contents of the liver. Inactivation of Kupffer cells with gadolinium chloride or depletion of neutrophils with cyclophosphamide relieved cadmium hepatotoxicity only in 6-month-old rats. In addition, 6-month-old rats were more susceptible than 2-month-old rats to lipopolysaccharide-induced hepatotoxicity. The results suggest that age-associated changes in Kupffer cell function and infiltration of neutrophils are important determinants of cadmium-induced hepatotoxicity in rats.
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PMID:Age-related change in cadmium-induced hepatotoxicity in Wistar rats: role of Kupffer cells and neutrophils. 970 82

Total superoxide dismutase (SOD, EC 1.15.1.1) and catalase (CAT, EC 1.11.1.6) activities in erythrocytes and the glutamic acid-oxalacetic acid-transaminase (GOT, EC 2.6.1.1) and glutamic acid-pyruvic acid-transaminase (GPT, EC 2.6.1.2) activities in the plasma were measured in experimental groups of carps (Cyprinus carpio L.) exposed to cadmium in a concentration of 20 mg Cd/l water under aquarium conditions for 6, 12, 18 and 24 hours and in control fishes. It was shown that the total activity of SOD in the erythrocytes is significantly decreased after 12, 18 and 24 hours of cadmium exposure. Increased activities of CAT (after 24 hours) in the erythrocytes and GOT and GPT in the plasma were found in cadmium-treated fishes. At the same time the concentration of blood haemoglobin and haematocrit values were significantly diminished. These results indicate that cadmium causes oxidative stress and tissue damage in the exposed fishes.
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PMID:Activities of superoxide dismutase and catalase in erythrocytes and transaminases in the plasma of carps (Cyprinus carpio L.) exposed to cadmium. 972 86

Pollution and industrial practices result in concentrations of metals and other environmental agents that are related to environmental toxicity. A rat bioassay was utilized for the identification of toxic effects of cadmium intake. This demonstrated increased total urinary proteins and increased kidney weights in rats exposed to CdCl2 for 7 days, in drinking water (100 mg/L). Serum creatinine, total and direct bilirubin concentrations and alanine transaminase activity were increased in Cd-exposed rats, indicating renal and hepatic toxicity. It was also observed that lipoperoxide concentrations were increased, while Cu-Zn superoxide dismutase activity was decreased in rats treated with cadmium. This indicated that the renal and hepatic toxicity induced by cadmium involved superoxide radicals.
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PMID:Risk assessment of cadmium toxicity on hepatic and renal tissues of rats. 984 8

Activated sludge is a rich source of nitrogenous matter and has been recommended as cheap supplement in animal feed. It has been incorporated into cattle and poultry feed. It is well known that sewage of purely domestic origin is also contaminated with heavy metals, pesticides, and other organic pollutants. A study was undertaken to determine the toxic effects of heavy metal-contaminated domestic sewage sludge on young male Wistar rats by supplementing dehydrated activated sludge in their diet at concentrations of 5, 10, 15 and 20%. The sludge was found to be contaminated with 1.820 (zinc), 0.273 (nickel), 0.017 (lead), 0.053 (copper), 0.006 (chromium), and 0.005 (cadmium)mg/g of dry sludge, by analysis by atomic absorption spectroscopy. The toxic effects of sludge-supplemented diets on individual groups of rats were assessed by assaying various enzyme activities in serum, liver, muscle, and brain. Levels of serum and liver alanine aminotransferase and succinate dehydrogenase (SDH) were significantly low in all the sludge-supplemented diet-fed (SSDF) rats. Similarly, serum lactate dehydrogenase (LDH) and muscle SDH activity were also significantly reduced in the SSDF rats. On the other hand, liver and muscle LDH, serum and liver aspartate aminotransferase, and serum and muscle alkaline phosphatase activities were significantly higher in all the SSDF animals. Brain and muscle acetylcholinesterase activity was significantly high in all the SSDF groups. This study indicates that even though the sludge is a rich source of nitrogenous matter, its supplementation in poultry and animals feed should be done with caution. Otherwise, the contaminants found in the sludge will biomagnify in the food chain and lead to various toxicological hazards.
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PMID:A study of toxic effects of heavy metal contaminants from sludge-supplemented diets on male Wistar rats. 1005 66

The accumulation of cadmium, copper and lead and their effects on aspartate and alanine aminotransferases in digestive gland, gills, foot and soft body in the clam Ruditapes philippinarum were examined. The animals were exposed to different concentrations: Cd (200-600 micrograms.l-1), Pb (350-700 micrograms.l-1) and Cu (10-20 micrograms.l-1) for 7 days. The highest concentrations were found in digestive gland for cadmium and copper, and in gills for lead, and the lowest values were observed in the foot. Aspartate aminotransferase activity (AST), in general, was not inhibited by cadmium, lead or copper during the exposure. Only in clams exposed to cadmium (600 micrograms.l-1, 7 days) and copper (20 micrograms.l-1, 5 days) were observed significant differences (P < 0.05) in foot and gills, respectively, with respect to control. In the case of alanine aminotransferase activity (ALT), significant differences were observed for cadmium and lead in treated animals with respect to control. With regard to copper, a decrease in ALT was observed in gills and foot exposed to 20 micrograms.l-1. A significant correlation (P < 0.05) was observed between ALT and metal accumulation for cadmium, copper and lead in gills. In the case of soft body, only cadmium and lead showed a significant correlation. In summary, R. philippinarum can be considered a bioindicator species for cadmium and lead accumulation and ALT could be useful as biomarker of sublethal stress for these metals in soft tissues and gills can be considered an adequate target tissue for copper.
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PMID:Effect of heavy metals (Cu, Cd and Pb) on aspartate and alanine aminotransferase in Ruditapes philippinarum (Mollusca: Bivalvia). 1019 53


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