Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nickel, a major environmental pollutant is known for its clastogenic, toxic and carcinogenic potentials. The present investigation shows that ellagic acid proves to be exceptional in the amelioration of the nickel-induced biochemical alterations in serum, liver and kidney. Administration of nickel (250 micromol Ni/kg body wt) to female Wistar rats, resulted in increase in the reduced glutathione (GSH) content [kidney (*P<0.05) and liver (**P<0.001)] and Glutathione-S-transferase (GST) and glutathione reductase (GR) activities [kidney and liver, (**P<0.001)]. Ellagic acid treatment to the intoxicated rats leads to the formation of soluble ellagic acid-metal complex which facilitates excretion of nickel from the cell or tissue, thus ameliorating nickel-induced toxicity, as evident from the down regulation of GSH content, GST and GR activities with concomitant restoration of glutathione peroxidase (GPx) activity in liver and kidney. Our data shows that ellagic acid maintains cell membrane integrity through sequestration of metal ions from the extracellular fluid, as evident from the alleviated levels of serum glutamate oxaloacetate transaminase, (SGOT), serum glutamate pyruvate transaminase (SGPT) and lactate dehydrogenase (LDH) when compared to nickel treated group. Similarly, the enhanced blood urea nitrogen (BUN) and serum creatinine levels that are indicative of renal injury showed a reduction of about 45 and 40%, respectively. The data also show that treatment of ellagic acid after 30 min of nickel administration exhibits maximum inhibition in a dose-dependent manner. In summary, our data suggests that ellagic acid act as an effective chelating agent in suppressing nickel-induced renal and hepatic biochemical alterations.
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PMID:Ellagic acid ameliorates nickel induced biochemical alterations: diminution of oxidative stress. 1060 94

In 1985 a 19-year old patient developed small, reddish exudative boils on the on the torso and proximate extremities that healed leaving a brownish hyperpigmentation. A 5-week stay in a dermatological clinic showed only an epicutaneous nickel sensitivity: multiform exudative erythema ID-reaction under epicutaneous nickel sensitivity. After release following antibiotic and combined steroid therapy the alterations soon receded while on nickel-free diet. She had taken a 3-phase preparation containing norethisterone and ethinylestradiol. After discontinuation of the pill in 1987 no new pustule formation occurred and both lower leg erosions healed. She was a nullipara who smoked 20 cigarettes a day and drank lightly. Increased glutamic-oxaloacetic transaminase (GOT) of 24 U/1 and glutamic-pyruvic transaminase (GPT) of 44 U/1, border values of serum iron of 175 mg/dl and cholesterol of 272 mg/dl, and massive thrombocytosis of 384.000/mcg and massive leukocytosis of 11.000/mcl were found. After 1 week all these values returned to normal except for a slightly higher GPT value of 24 U/1. After complete abstinence from allergens and fasting for 5 days, an iodine provocation test to prove the suspicion of dermatitis herpetiformis proved negative. After release she agreed to take a few tablets which again resulted in vesicular eruptions mostly on the abdomen and back that promptly healed after quitting the pills. Herpes gestations could not be shown in the blood. The use of the pill has become so prevalent that it is often forgotten that it is an agent that can contribute to unclear clinical symptoms.
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PMID:[Herpes gestationis acquired during oral contraceptive use]. 1228 89

Some aspects of protein metabolism were studied in foot, hepatopancreas and mantle tissues of snail, Pila globosa on exposure to lethal concentration for 2 days (336.7 mg/L) and sublethal concentration (67.34 mg/L) of nickel for 1, 5 and 10 days. Total, structural and soluble proteins decreased significantly and to continence, this the levels of amino acids and protease activity increased in all the tissues of snail at all time points examined. Activities of AAT (Aspartate aminotransferase) and AlAT (Alanine aminotransferase) showed contrasting trends of inhibition and elevation during lethal and sublethal concentrations of nickel treatment. GDH (Glutamate dehydrogenase) activity was increased in all the tissues with increase in exposure time. Level of ammonia decreased in snails at sublethal concentration, but increment was observed in lethal concentration along with increased urea content. Under lethal and sublethal exposures, the changes in all the parameters were more pronounced in hepatopancreas followed by foot and mantle. At most instances, snails in the lethal medium were affected more compared to sublethal concentration.
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PMID:Nickel induced changes on some aspects of protein metabolism in the tissues of Pila globosa. 1297 14

Nickel has an adverse effect on some aspects of protein metabolism of the freshwater fish, Cyprinus carpio. The main changes observed were: (a) Decrease in soluble, structural and total proteins, AlAT and AAT activities with an increase in the levels of free amino acids, protease and GDH activities and ammonia in the gill and kidney at 1, 2, 3, and 4 days of exposure to a lethal concentration, 40 mg litre(-1) of nickel; (b) Increase in soluble, structural and total proteins, free amino acids and the activities of protease, AlAT, AAT and GDH with a decrease in ammonia and urea in these organs at 1, 5, 10 and 15 days of exposure to sublethal concentration, 8 mg litre(-1); (c) The magnitude in these changes increased over time with both concentrations of the metal, and was more marked in gill than in kidney.
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PMID:Effect of nickel on some aspects of protein metabolism in the gill and kidney of the freshwater fish, Cyprinus carpio L. 1509 78

Broiler chicken and rabbit experiments were carried out to study the effects of nickel (Ni) supplementation on growth performance and Ni metabolism. ROSS cockerels and New Zealand White female rabbits were fed a diet containing Ni in concentrations of 0, 50 and 500 mg/kg in dry matter (DM). Dietary supplementation of 50 mg Ni/kg slightly improved the body weight gain (BWG) and had a beneficial effect on the feed conversion efficiency (FCE) in broiler chickens. However, Ni added at a level of 500 mg/kg significantly (P < 0.05) reduced the BWG by 10% and resulted in significantly (P < 0.05) worse (2.3 +/- 0.2 kg/kg) FCE. The relative weight of the liver in cockerels was significantly (P < 0.05) decreased by Ni as compared to the control group (1.7 and 2.1% vs. 2.6%). The activity of AST and CHE enzymes was increased insignificantly by dietary supplementation of 500 mg Ni/kg, indicating damage of the liver parenchyma. The results of serum biochemistry were confirmed by a mild or moderate form of pathological focal fatty infiltration of the liver in broilers. Supplemental Ni of 50 mg/kg concentration resulted in non-significantly increased BWG in rabbits. Ni added to the diet at a level of 500 mg/kg reduced the digestibility of crude protein by 3-4% and that of crude fibre by 20-25% in rabbits. Approx. 98% of the ingested Ni was lost from the body via the faeces, 0.5-1.5% via the urine and approx. 1% was incorporated into the organs of rabbits. As a result of dietary supplementation of 50 and 500 mg Ni/kg, Ni accumulated in the kidneys (4.9 +/- 0.5 and 17.1 +/- 3.1 vs. 1.9 +/- 0.3 mg/kg DM), ribs (10.3 +/- 0.4 and 10.4 +/- 0.6 vs. 9.1 +/- 0.6 mg/kg DM), heart (1.4 +/- 0.2 and 2.5 +/- 0.4 vs. 1.0 +/- 0.1 mg/kg DM) and liver (1.3 +/- 0.1 and 2.2 +/- 0.2 vs. 0.9 +/- 0.05 mg/kg DM), as compared to the control animals. It can be stated that supplementation of the diet with 50 mg Ni/kg had slight but non-significant beneficial effects on the growth performance of broiler chickens and rabbits.
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PMID:Effects of nickel supply on the fattening performance and several biochemical parameters of broiler chickens and rabbits. 1516 50

This study was planned to determine the protective role of zinc, if any, in attenuating the toxicity induced by nickel sulfate in rat liver. Female Sprague Dawley (SD) rats received either nickel alone in the dose of 800 mg/l in drinking water, zinc alone in the dose of 227 mg/l in drinking water, and nickel plus zinc or drinking water alone for a total duration of eight weeks. The effects of different treatments were studied on various parameters in rat liver which include antioxidant enzymes, levels of nickel and zinc and histoarchitecture at the light microscopic level. Further, the activities of hepatic marker enzymes AST and ALT were also studied in rat serum. Nickel treatment to the normal control animals, resulted in a significant increase in lipid peroxidation and enzyme activities of catalase and glutathione-S-transferase. On the contrary, nickel treatment to normal rats caused a significant inhibition in the levels of reduced glutathione. Superoxide dismutase activity was found to be decreased which however was not significant. Interestingly, when Zn was supplemented to nickel treated rats, the activities of catalase, and glutathione-S-transferase and the levels of GSH and lipid peroxidation came back to within normal limits. Activities of serum AST and ALT were increased significantly following nickel treatment to normal rats. Simultaneous zinc administration to nickel treated rats tended to restore the altered levels of AST and ALT. Normal control and zinc treated animals revealed normal histology of liver. On the other hand, nickel treated animals showed alterations in normal hepatic histoarchitecture which comprise of vacuolization of the hepatocytes and dilatation of sinusoids as well as increase in the number of bi-nucleated cells. Administration of zinc to nickel treated rats resulted in marked improvement in the structure of hepatocytes, thus emphasizing the protective potential of zinc in restoring the altered hepatic histoarchitecture. The nickel administration to normal rats indicated increased concentrations of nickel and decreased concentrations of zinc. However, zinc effectively brought the altered levels of nickel and zinc to within normal range. The study concludes that zinc has the potential in alleviating the toxic effects of nickel in rat liver because of its property to induce metallothionein (S-rich protein) as a free radical scavenger, or its indirect action in reducing the levels of oxygen reactive species.
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PMID:Protective role of zinc in nickel induced hepatotoxicity in rats. 1553 90

This study was designed to determine the toxic effects of nickel sulfate on the biochemical and elemental profile of liver in protein deficient rats. Nickel sulfate in the dose of 800mg/l in drinking water was administrated to Sprauge Dawley (S.D) normal control as well as protein deficient rats for a total duration of eight weeks. The effects of nickel treatment and protein deficiency when given separately and in combination were studied on rat liver marker enzymes like Alkaline phosphatase (ALP),Glutamate oxaloacetate transaminase (GOT), Glutamate pyruvate transaminase (GPT) and also on the status of essential elements in rat liver. Protein deficient, Ni treated as well as combined protein deficient and nickel treated rats showed significant reductions in the body weight and hepatic protein contents as compared to normal control rats. Hepatic alkaline phosphatase activity and alanine aminotransferase showed a significant elevation in rats subjected to protein deficiency, nickel treatment and combined protein deficiency and nickel treatment. As regards to hepatic levels of aspartate aminotransferase a significant elevation was observed in protein deficient and nickel treated protein deficient animals. Nickel administration to normal and protein deficient rats has resulted in a significant increase in concentrations of nickel, phosphorus and sulfur in liver tissue. The concentration of zinc and copper in liver tissue decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals. Tissue iron concentrations were found to be decreased in protein deficient animals, but the concentrations of iron got elevated significantly in nickel treated and nickel treated protein deficient animals. It has been observed that selenium got decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals when compared to normal animals. The elevation of selenium in nickel treated protein deficient animals was also significantly higher when compared to protein deficient animals.
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PMID:Ineffectiveness of nickel in augmenting the hepatotoxicity in protein deficient rats. 1633 21

In the current study, we examined whether subchronic exposure via drinking water to low doses of a mixture of metals (arsenic, cadmium, lead, mercury, chromium, manganese, iron, and nickel), found as contaminants in various water sources of India, and to concentrations equivalent to WHO maximum permissible limits (MPL) in drinking water for individual metals, can alter systemic physiology of male rats. Data on water contamination with metals in India were collected from the literature and metals were selected on the basis of their frequency of occurrence and contamination level above MPL. Male Wistar rats were exposed to the mixture at 0, 1, 10, and 100 times the mode concentrations (the most frequently occurring concentration) of the individual metals via drinking water for 90 days. One more group of rats was exposed to the mixture at a concentration equivalent to the MPL (WHO) in drinking water for individual metals. Toxic potential of the mixture was evaluated by assessing general toxicological end points, serum chemistry and histopathology of vital organs. The mixture decreased body weight and water consumption and increased weights of brain, liver, and kidneys with 10x and 100x doses. After 30 days of exposure, no appreciable changes were found in any blood clinical markers. After 60 days, only the 100x dose, while after 90 days both 10x and 100x doses increased activities of aspartate aminotransferase and alkaline phosphatase and levels of urea nitrogen and creatinine and decreased total protein and albumin levels, but alanine aminotransferase activity and glucose level were not affected. At 10x and 100x exposure levels, qualitatively similar, but dose-dependent vascular, degenerative, and necrotic changes were observed in brain, liver, and kidney. The results indicate that subchronic exposure to the metal mixture affected general health of male rats by altering the functional and structural integrity of kidney, liver, and brain at 10 and 100 times the mode concentrations of the individual metals in Indian water sources, but exposure at mode concentrations of contemporary water contamination levels or at concentrations equivalent to the MPL for individual metals in drinking water may not cause any health hazards in male rats.
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PMID:Effects of subchronic exposure via drinking water to a mixture of eight water-contaminating metals: a biochemical and histopathological study in male rats. 1788 70

Nickel (Ni), a major environmental pollutant, is known for its wide toxic manifestations. In the present study caffeic acid (CA), one of the most commonly occurring phenolic acids in fruits, grains and dietary supplements, was evaluated for its protective effect against the Ni induced oxidative damage in liver. In this investigation, Ni (20 mg/kg body weight) was administered intraperitoneally for 20 days to induce toxicity. CA was administered orally (15, 30 and 60 mg/kg body weight) for 20 days with intraperitoneal administration of Ni. Ni induced liver damage was clearly shown by the increased activities of serum hepatic enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT) and lactate dehydrogenase (LDH) along with increased elevation of lipid peroxidation indices (thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides). The toxic effect of Ni was also indicated by significantly decreased levels of enzymatic (superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (glutathione (GSH), vitamin C and vitamin E). CA administered at a dose of 60 mg/kg body weight significantly reversed the activities of hepatic marker enzymes to their near normal levels when compared with other two doses. In addition, CA significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. All these changes were supported by histological observations. The results indicate that CA may be beneficial in ameliorating the Ni induced oxidative damage in the liver of rats.
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PMID:Efficacy of caffeic acid in preventing nickel induced oxidative damage in liver of rats. 1840 91

The purpose of this study was to determine certain blood biochemical parameters in hens of Isa Brown breed (n = 20) after nickel administration. Animals were divided into four groups (K, P1, P2, P3). Experimental hens (n = 5; in each group) received nickel (NiCl2) as peroral administration in drinking water in various doses (P1 - 0.02 g NiCl2/L; P2 - 0.2 g NiCl2/L; P3 - 2.0 g NiCl2/L of drinking water) for 28 days. The last group - K (n = 5) was the control, receiving no nickel. Biochemical parameters of mineral profile (calcium; phosphorus; magnesium; sodium; potassium) and of energy and enzymatic profile [(glucose; total cholesterol; total proteins; triglycerides; alanine aminotransferase (ALT) aspartate aminotransferase (AST) gamma glutamyl transferase (GGT) and glutamatdehydrogenase (GLDH)] were analyzed in blood serum on Day 0, 7, 14, 21 and 28 of the experiment. Average levels of mineral metabolism parameters were relatively stable apart from calcium. The evaluation registered a significant decrease in calcium during the experiment mainly in the group with highest nickel concentration in drinking water. No significant differences were detected between groups in energy and enzymatic profile apart from the concentrations of ALT on Day 7. In conclusion, there were significant associations between nickel levels and calcium and ALT in blood serum of the hens. No significant differences were detected in other biochemical parameters of mineral profile (P, Mg, Na, K) and energy and enzymatic profile (glucose, total cholesterol, total proteins, triglycerides, AST, GGT and GLDH) after nickel administration. Our results may contribute to an evaluation of reference levels of analyzed parameters, to monitor the health and nutritional status of hens. In this study also the negative effect of nickel mainly on calcium metabolism was detected.
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PMID:Nickel-induced blood biochemistry alterations in hens after an experimental peroral administration. 1880 18


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