Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human intrahepatic biliary epithelial cells are important immune targets in a variety of hepatobiliary diseases particularly primary biliary cirrhosis and primary sclerosing cholangitis. The ability to isolate and maintain these cells in short term primary tissue culture has permitted us to develop an in vitro cytotoxicity assay for the study of these cells as potential targets to a variety of toxic stimuli. We have therefore established a chromium-51 (51Cr) release cytotoxicity assay for use with primary cultures of human intrahepatic biliary epithelial cells. The method is simple, reproducible and is more sensitive than dye exclusion, light microscopy and release of lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase.
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PMID:A 51Cr release cytotoxicity assay for use with human intrahepatic biliary epithelial cells. 167 52

Beating rat heart cultures were prepared in vitro and infected with Coxsackie B-2 virus. The cells were evaluated in the post-infected period for changes in cardiac enzymes, alterations in beating frequency and cytotoxicity as measured by chromium 51 (51Cr) release. The cardiac enzymes, lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) were measured in infected and uninfected controls over a period of 120 h. Enzyme levels in the infected cells remained essentially the same for the first 42 h as compared to the controls. At this time, the LDH levels increased rapidly reaching 116 +/- 24.8 U/l while the controls remained at 46.9 +/- 9.7 U/l. Aspartate aminotransferase levels increased at a slower rate and obtained a level of 104 +/- 20.2 U/l compared to 66.6 +/- 13.2 U/l in the control. Visual evidence of cellular damage as measured by decreased beating frequencies and the appearance of cytopathic effect was first noted at 42 h post-infection. Complete loss of cardiac beats and maximal viral cytopathic effect occurred at 96 h post-infection. Cardiac cellular damage as measured by cytotoxicity assay was found to parallel those changes seen in cardiac enzymes. No significant changes in cytotoxicity were observed for the first 24 h; however, at 48 h increased release of 51Cr was noted and visual evidence of viral replication also was present. The cardiac enzyme changes noted in beating rat heart cells appear to be similar to those changes reported in patients with viral-induced myocardial disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coxsackie B-2 virus infection in rat beating heart cell culture. 300 12

Hepatotoxic effects of chromium have been studied on the liver function enzymes of male New Zealand white rabbits, Oryctolagus cuniculus, with and without pretreatment with phenobarbitone (PB) and promethazine (PM). The total body weight was decreased under all experimental conditions. After PB administration (5 mg/kg body wt/day for 5 days), the serum glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), lactate dehydrogenase (LDH), and isocitrate dehydrogenase (ICDH) activities decreased 21%, 65%, 25%, and 37%, respectively, whereas the alkaline phosphatase (AP) activity increased 70%. After PM treatment (5 mg/kg body wt/day for 5 days) the serum GPT was inhibited 73%, whereas LDH activity was increased 37%. The hepatic GPT and AP activities decreased after PB (52% and 31%, respectively), and PM (48% and 44%, respectively) treatments, whereas the activities of LDH and ICDH increased (after PB: 817% and 109%, respectively, and after PM: 136% and 44%, respectively). Potassium dichromate, administered at a dose of 8 mg/kg body wt/day for 5 days, decreased serum GOT (44%), GPT (61%), LDH (63%), and AP (44%) activities. The hepatic GOT, GPT and AP activities were likewise decreased (86%, 51%, and 46%, respectively), whereas hepatic LDH and ICDH activities increased 667% and 193%, respectively. When administered to PB-pretreated animals, the serum GOT and AP activities were decreased (50% and 68%), whereas ICDH was increased (29%). The hepatic GOT, LDH, and ICDH activities increased 79%, 221%, and 130%, respectively. In the PM-pretreated animals, the chromium treatment inhibited the activities of serum GOT (48%), GPT (44%), and LDH (43%). The hepatic GPT, LDH, and ICDH activities increased 90%, 133%, and 52%, respectively.
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PMID:Sublethal effects of hexavalent chromium on the body growth rate and liver function enzymes of phenobarbitone-pretreated and promethazine-pretreated rabbits. 925 33

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 ability of chromium (Cr) salts to increase metallothionein (MT) levels in rat liver, kidney and pancreas, and its relationship with the presence of toxic effects are reported here. Rats were injected subcutaneously with 0, 10, 20, 30, 40, or 50 mg K2Cr2O7/kg and sacrificed 24 h later. Total Cr accumulation followed a dose-dependent pattern, levels in kidney being higher than those in liver or pancreas, suggesting different tissue bioavailabilities and accumulation patterns. Cr(IV) administration resulted in a tissue-specific MT induction: pancreas and liver showed five- and 3.5-fold MT increases, respectively; no increase was observed in the kidney. A positive correlation was observed between zinc and MT concentrations in liver, and between total Cr and MT concentrations in pancreas. Serum alpha-amylase activity showed a dose-dependent increase starting from 20 mg/kg, whereas serum glucose levels increased at doses higher than 30 mg/kg. Serum aspartate aminotransferase and alanine aminotransferase activities were increased in a dose-dependent manner, from 20 and 30 mg/kg, respectively. Our results showed that treatment with Cr(VI) can induce MT synthesis in pancreas and suggests a subsequent binding of Cr to MT. Also, pancreas is a target organ for Cr toxicity, and the usefulness of alpha-amylase activity as a sensitive biomarker of Cr toxicity in human exposed populations merits further study.
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PMID:Chromium increases pancreatic metallothionein in the rat. 1068 10

Deleterious effects of chromium (VI) compounds are diversified affecting almost all the organ systems in a wide variety of animals. Therefore, the present study was carried out to determine the effectiveness of folic acid (FA) in alleviating the toxicity of chromium (VI) on certain biochemical parameters, lipid peroxidation, and enzyme activities of male New Zealand white rabbits. Six rabbits per group were assigned to one of four treatment groups: 0 mg FA and 0 mg Cr(VI)/kg BW (control); 8.3 microg FA/kg BW; 5 mg Cr(VI)/kg BW; 5 mg Cr(VI) plus 8.3 microg FA/kg BW, respectively. Rabbits were orally administered their respective doses every day for 10 weeks. Results obtained showed that Cr(VI) significantly (P < 0.05) increased the levels of free radicals and the activity of glutathione S-transferase (GST), and decreased the content of sulfhydryl groups (SH groups) in liver, testes, brain, kidney, and lung. The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP), and lactate dehydrogenase (LDH) were significantly decreased in liver and testes due to Cr(VI) administration. Also, AlP and AcP activities were significantly decreased in kidney and lung. The activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma. Contrariwise, the activities of AST and ALT were significantly increased in plasma, while AlP and AcP decreased. Chromium (VI) treatment caused a significant decrease in plasma total protein (TP) and globulin, and increased total lipids (TL), cholesterol, glucose, urea, creatinine, and bilirubin concentrations. Folic acid alone significantly decreased the levels of free radicals in liver, brain, and kidney, and increased the content of SH-group. The activities of AST, ALT, and LDH in liver; AST, ALT, AlP, AcP, and LDH in testes; AcP in kidney; AlP and AcP in lung, and LDH in brain were significantly increased. Plasma TP and albumin were increased, while urea and creatinine were decreased. The presence of FA with Cr(VI) restored the changes in enzyme activities and biochemical parameters. In conclusion, folic acid could be effective in the protection of chromium-induced toxicity.
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PMID:Biochemical study on the protective role of folic acid in rabbits treated with chromium (VI). 1678 79

The effect of fly ash inhalation (4h daily, 5 days a week) for 28 days on the deposition of metal ions and histopathological changes in the liver and serum clinical enzymes has been studied. The results showed an increase in the concentration of metals such as cadmium (Cd), chromium (Cr), copper (Cu), manganese (Mn), and lead (Pb) in the tissues of exposed rats. The level of metals varied from metal to metal and from organ to organ. Level of serum enzymes such as serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, and alkaline phosphatase were increased in fly ash exposed rats using whole body inhalation exposure as compared to sham controls. Histopathological studies of rat liver exposed to fly ash revealed infiltration of mononuclear cells in and around the portal triads, which seems to be laden with fly ash particles. Hepatocytes showed necrotic changes such as pyknotic nuclei, karyorrhexis, and karyolytic. These changes were more towards the centrolobular areas than the midzonal and periportal areas. These findings demonstrate that the toxic metals of inhaled fly ash in rats may get translocated into extrapulmonary organs, become deposited and hence may manifest their toxic effects on different tissues.
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PMID:Effect of fly ash inhalation on biochemical and histomorphological changes in rat liver. 1716 87

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

Fish serum may reflect status of many biochemical processes in the metabolism. Heavy metals, as environmental stressors, may alter serum biochemical parameters in fishes. Thus, freshwater fish, Oreochromis niloticus, were exposed to low levels (0.05 mg/L) of metals (silver [Ag], cadmium [Cd], copper [Cu], chromium [Cr], zinc [Zn]) to investigate responses of serum biochemical parameters over different exposure periods (0, 5, 10, 20, 30 d). Fish mortality occurred only in Ag exposure, as all fish died between days 12 to 16. Activities of alkaline phosphatase (ALP), alanine transaminase (ALT), and aspartate transaminase (AST) were altered only in Cu- and Cd-exposed fish. Both Cd and Cu exposures decreased the activity of ALP, although they increased the activities of ALT and AST. Glucose concentrations increased in Ag-, Cd-, and Cu-exposed fish, with a sharp increase occurring in Ag-exposed fish before mortality began. Total protein and triglyceride concentrations increased in Ag-exposed fish, although they decreased in Cu-exposed ones. However, all metal exposures increased cholesterol concentration in the serum. Concentration of blood urea nitrogen increased in Ag-, Cd-, and Cu-exposed fish, although it decreased in Cr-exposed ones. Calcium level decreased only in Cu-exposed fish, and Cl(-) level decreased in Ag-exposed fish. Silver and Cu exposures also decreased Na(+) level in the serum. Cadmium and Cu exposures increased serum K(+) levels. The present study, investigating the effects of environmentally realistic metal exposures on serum biochemical parameters, demonstrated that fish serum could sensitively reflect environmental metal stress. Thus, it suggests that serum biochemical parameters could be used as important and sensitive biomarkers in ecotoxicological studies concerning the effects of metal contamination and fish health.
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PMID:Changes in serum biochemical parameters of freshwater fish Oreochromis niloticus following prolonged metal (Ag, Cd, Cr, Cu, Zn) exposures. 1834 36

Chromium (VI) compounds are genotoxic and carcinogenic in a variety of experimental systems. Garlic and its derivatives possess antioxidant properties to scavenge the toxic radicals. The mechanism by which garlic induces the antioxidant and phase II enzymes during oxidative stress-induced apoptosis is not known. This study aims to evaluate the protective role of aqueous garlic extract (AGE; 200 mg kg(-1) b.w.) and S-allylcysteine (SAC; 100 mg kg(-1) b.w.) on potassium dichromate-induced apoptosis and oxidative stress in the hepatocytes of Wistar rats. Activities of liver marker enzymes such as aspartate transaminase, alanine transaminase and lactate dehydrogenase were found to be increased in the serum of chromium-induced group, whereas administration of garlic extract and SAC restored the enzymes to near normal status. The activities of enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase), non-enzymic antioxidants (vitamin C and vitamin E) and the levels of reduced glutathione were found to be decreased, while an increase in lipid peroxidation (LPO) and reactive oxygen species were observed in the liver tissues of chromium-induced group. Administration of AGE and SAC reversed the status of these parameters substantially. Histological and transmission electron microscopic studies support our findings. Confocal microscopic analysis using annexin-V showed the involvement of apoptosis. Further, the expression of a novel transcription factor, nuclear factor-E2 related factor 2 (Nrf2) was investigated using Immunofluorescence and Western blotting. The results show the promising role of Nrf2-mediated antioxidant defense of AGE and SAC against chromium toxicity.
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PMID:Chromium (VI)-induced oxidative stress and apoptosis is reduced by garlic and its derivative S-allylcysteine through the activation of Nrf2 in the hepatocytes of Wistar rats. 1854 44


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