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)

The present study was undertaken to investigate the effects of acute 2,4-dichlorophenoxyacetic acid (2,4-D) intoxication (0.6 g/kg, po) on lactate dehydrogenase, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, amylase, creatinine, glucose, total protein and albumin levels in rats. Serum levels of lactate dehydrogenase, alkaline phosphatase and creatinine increased from 1- to 4-fold at 5, 8 and 24 h after 2,4-D administration, whereas serum levels of aspartate and alanine aminotransferase were higher only at 8 and 24 h. Amylase levels were only increased 8 h after administration of 2,4-D and then returned to normal levels. In contrast, 2,4-D reduced the serum levels of glucose and total protein 5, 8 and 24 h and serum albumin levels 5 h after herbicide intoxication. Thus, acute intoxication with 2,4-D disrupts serum levels of several enzymes and components which are considered to be indicators of tissue injury. Most likely these alterations mainly reflect hepatic and muscle tissue damage induced by the herbicide, but significant pancreatic and kidney toxicity may also have occurred.
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PMID:Effects of acute 2,4-dichlorophenoxyacetic acid intoxication on some rat serum components and enzyme activities. 172 51

Wofatox 50 EC (methylparathion 50%), Nevifosz 50 EC (phosmethylan 50%), Kolfugo 25 FW (carbendazim 25%) and Dikamin D (2,4-D 40%) pesticide formulations were used as test material. The incubated chicken eggs were directly exposed to the applied pesticides with injection into the air cell. Blood samples were obtained and some plasma parameters including packed cell volume (PCV), total protein, glucose, cholesterol, aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and plasma pseudocholinesterase (PChE) activities were evaluated. Although the mortality rate obtained for the treated and control groups did not differ, there were significant changes in plasma biochemistry in relation to pesticide treatment. The present paper attempts to help those undertaking embryological and teratological studies on avian embryos exposed to pesticides including studies on changes occurring in certain plasma parameters.
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PMID:Changes in blood plasma biochemistry of chicken embryos exposed to various pesticide formulations. 262

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D) was studied in cattle. Steers were dosed po with 100, 300 or 600 mg 2,4-D/kg bw. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), O-glutamyl transferase (O-GT), creatine kinase (CK), lactate dehydrogenase (LDH) activities and urea, creatinine, glucose, total proteins and albumin levels were determined at intervals after dosing. The lowest 2,4-D dose did not change the biochemical parameters studied; the 300 mg/kg dose decreased AST, O-GT and CK activities and increased urea and glucose levels; the highest dose of 2,4-D increased LDH and CK activities and protein, urea, creatinine and glucose levels. These changes were time and dose-dependent and completely reversible. Acute 2,4-D intoxication disrupted the serum levels of several enzymes and blood components which mainly reflect kidney and muscle damage induced by the herbicide.
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PMID:Effects of acute 2,4-dichlorophenoxyacetic acid on cattle serum components and enzyme activities. 854 Feb 21

The acute, subchronic and chronic toxicities of 2,4-dichlorophenoxyacetic acid (2,4-D) were studied ir rats. Animals were exposed acutely (600 mg/kg), subchronically (200 ppm for 30 d) and chronically (200 ppm for 180 d) to 2,4-D by the oral route. Clinical, laboratory and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased locomotor activity and induced ataxia, sedation, muscular weakness (mainly of the hind quarters) and gasping for breath; increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), amylase activities and creatinine levels; decreased total protein (TP) and glucose levels; and increased hematocrit values. Subchronic and chronic 2,4-D exposures did not induce overt clinical signs or symptoms of intoxication. However, subchronic herbicide exposure increased AST activity and albumin and hematocrit values, and chronic exposure increased AST, AP and LDH activities, decreased amylase and glucose levels, but did not change hematocrit values. Chromatographic analysis of the serum of chronically exposed rats showed the presence of the herbicide; the amount found (3.76 +/- 1.16 micrograms/ml) suggested the absence of 2,4-D accumulation within the body. Although macroscopic or histopathological lesions were not observed in acutely, subchronically or chronically 2,4-D exposed rats, the laboratory data obtained suggest tissue injuries after dosing, since the results are considered early indicators of primarily hepatic and muscle tissue damage.
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PMID:Acute, subchronic and chronic 2,4-dichlorophenoxyacetic acid (2,4-D) intoxication in rats. 888 38

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D), a herbicide, was studied in chicks dosed with 100, 300, 500, or 600 mg 2,4-D/kg BW, by the oral route. Clinical, laboratory, and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased motor activity and induced muscular weakness and motor incoordination; decreased weight gain; increased serum creatine kinase (CK) and alkaline phosphatase (AP) activities and serum uric acid (UA), creatinine (CR), and total proteins (TP) levels; and did not change serum aspartate aminotransferase (AST) or alanine aminotransferase (ALT) activities. These changes were time- and dose-dependent and reversible. The LD50 (lethal dose 50%) calculated for oral 2,4-D in chicks was 420 mg/kg BW (385 to 483). Chromatographic analysis of the serum of the intoxicated chicks showed the presence of the herbicide; the amount found was dose- and time-dependent, increasing from 2 to 8 h after exposure and decreasing afterwards. Histopathological post-mortem studies conducted on intoxicated chicks showed hepatic (vacuolar degeneration of the hepatocytes), renal (tubular nephrosis), and intestinal (hemorrhagic) lesions. Taken together, the observed alterations mainly reflected kidney and muscle tissue damage, although hepatic toxicity may also have occurred after acute 2,4-D intoxication.
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PMID:Acute 2,4-dichlorophenoxyacetic acid intoxication in broiler chicks. 956 31

This study aims to investigate the effects of the plant growth regulators (PGRs) (2,3,5-triiodobenzoic acid (TIBA), Naphthaleneacetic acid (NAA), and 2,4-dichlorofenoxyacetic acid (2,4-D)) on serum marker enzymes (aspartate aminotransferase (AST), alanin aminotransferase (ALT), creatine phosphokinase (CPK), and lactate dehydrogenase (LDH)), antioxidant defense systems (reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST), and catalase (CAT)), and lipid peroxidation content (malondialdehyde = MDA) in various tissues of rats. 50 and 100 ppm of PGRs as drinking water were administered orally to rats (Sprague-Dawley albino) ad libitum for 25 days continuously. The PGRs treatment caused different effects on the serum marker enzymes, antioxidant defense systems, and the MDA content in experimented rats compared to controls. Results showed that TIBA caused a significant decrease in serum AST activity with both the dosage whereas serum CPK was significantly increased with 100 ppm dosage of TIBA. Meanwhile, serum AST, CPK, and LDH activities were significantly increased with both dosage of NAA and 2,4-D. The lipid peroxidation end-product MDA significantly increased in the all tissues treated with both dosages of PGRs without any change in the brain and erythrocyte of rats treated with both the dosages of 2,4-D. The GSH depletion in the kidney and brain tissues of rats treated with both dosages of PGRs was found to be significant. Furthermore, the GSH depletion in the erythrocyte of rats treated with both dosages of PGRs except 50 ppm dosage of 2,4-D was significant too. Also, the GSH level in the liver was significantly depleted with 50 ppm of 2,4-D and NAA, whereas the GSH depletion in the same tissue did not significantly change with the treatment. The activity of antioxidant enzymes was also seriously affected by PGRs; SOD significantly decreased in the liver, heart, kidney, and brain of rats treated with both dosages of NAA, whereas the SOD activity in the erythrocytes, liver, and heart was either significantly decreased or not changed with two doses of 2,4-D and TIBA. Although the CAT activity significantly increased in the erythrocyte and brain of rats treated with both doses of PGRs, it was not changed in the liver, heart, and kidney. Meanwhile, the ancillary enzyme GR activity significantly increased in the brain, heart, and liver but decreased in the erythrocyte and kidney of rats treated with both doses of PGRs. The drug-metabolizing enzyme GST activity significantly increased in the heart and kidney but decreased in the brain and erythrocytes of rats treated with both dosages of PGRs. As a conclusion, the results indicate that PGRs might affect antioxidant potential enzymes, the activity of hepatic damage enzymes, and lipid peroxidation dose independently. Also, the rats resisted to oxidative stress via antioxidant mechanism but the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat's tissues. These data, along with the determined changes, suggest that PGRs produced substantial systemic organ toxicity in the erythrocyte, liver, brain, heart, and kidney during the period of a 25-day subacute exposure.
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PMID:Influence of subacute treatment of some plant growth regulators on serum marker enzymes and erythrocyte and tissue antioxidant defense and lipid peroxidation in rats. 1690 22

This study investigated the effects of 2,4-dichlorophenoxyacetic acid (2,4-D), a widely used herbicide, on the metabolism of goldfish, Carassius auratus, using only vital (non-lethal) approaches. After 96 h exposure to 1, 10 or 100 mg/L of 2,4-D selected hematological (total hemoglobin and hematocrit) and biochemical (glucose content, aspartate transaminase and acetylcholinesterase activities) parameters were unchanged in blood of exposed fish. At 100 mg/L of 2,4-D lymphocyte numbers decreased by 8%, whereas promyelocyte and metamyelocyte numbers increased by 7- and 2-fold, respectively. Exposure to 100 mg/L of 2,4-D also elevated carbonyl protein levels (by 2-fold), triglyceride content (by 43%) and alanine transaminase activity (by 46%) in goldfish plasma. All of these hematological and biochemical parameters reverted to control values after a 96 h recovery period. These data indicate that 2,4-D has toxicological effects on goldfish that can be monitored with multiple diagnostic tests using non-lethal blood testing.
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PMID:Goldfish can recover after short-term exposure to 2,4-dichlorophenoxyacetate: use of blood parameters as vital biomarkers. 2329 97

Detailed data from statistical analyses of the structural properties of the inter-domain linker peptides of the bacterial regulators of the family MocR are herein reported. MocR regulators are a recently discovered subfamily of bacterial regulators possessing an N-terminal domain, 60 residue long on average, folded as the winged-helix-turn-helix architecture responsible for DNA recognition and binding, and a large C-terminal domain (350 residue on average) that belongs to the fold type-I pyridoxal 5'-phosphate (PLP) dependent enzymes such aspartate aminotransferase. Data show the distribution of several structural characteristics of the linkers taken from bacterial species from five different phyla, namely Actinobacteria, Alpha-, Beta-, Gammaproteobacteria and Firmicutes. Interpretation and discussion of reported data refer to the article "Structural properties of the linkers connecting the N- and C- terminal domains in the MocR bacterial transcriptional regulators" (T. Milano, S. Angelaccio, A. Tramonti, M. L. Di Salvo, R. Contestabile, S. Pascarella, 2016) [1].
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PMID:Data from computational analysis of the peptide linkers in the MocR bacterial transcriptional regulators. 2766 76

2,4-Dichlorophenoxyacetic acid (2,4-D) is an extensively used herbicide in the field of agriculture, its ever-escalating use induces toxicity, health effects, and environmental impact. Oxidative stress plays a key role in pathogenesis of 2,4-D-induced liver and kidney damage. Magnesium (Mg) is a highly effective antioxidant agent in restoring oxidative damage by directly influencing the metabolic and physiological processes. Therefore, the present study aimed to evaluate Mg role in ameliorating the oxidative damages provoked by 2,4-D in rat model. Male Wistar rats (180-220 g) were distributed into four groups and treated intragastrically for 4 weeks. Group 1: control, group 2: 2,4-D (150 mg/kg body weight/day), group 3: simultaneously treated with 2,4-D (150 mg/kg body weight/day) and Mg supplement (50 mg/kg body weight/day), and group 4: Mg supplement (50 mg/kg body weight/day). Under experimental conditions, plasma hepatic and renal biomarkers, tissue oxidative status, and antioxidant enzymes activities were investigated. Results demonstrated that 2,4-D intoxication caused hepatic and renal impairments as indicated by the significantly increased (p < 0.001) alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, urea, creatinine, and blood urea nitrogen levels. In addition, 2,4-D caused a significant enhancement (p < 0.001) in the level of malondialdehyde as well as reduction (p < 0.001) of the superoxide dismutase, catalase, and glutathione reductase activities in both hepatic and renal tissues. Mg treatment prevented and reversed the toxic variations induced by 2,4-D. In general, these outcomes suggest that Mg may have antioxidant potential and ameliorative effects against 2,4-D provoking hepatic and renal toxicity in rat model.
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PMID:Magnesium supplementation ameliorates toxic effects of 2,4-dichlorophenoxyacetic acid in rat model. 3149 3