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 mechanisms by which heparin protects the liver during induced episodes of liver ischemia-reperfusion are poorly understood. Previous work in a swine model demonstrated that serum levels of glycohydrolases and lipid peroxide peaked within 3 h after 45 minutes of hepatic ischemia followed by reperfusion. Serum levels of lactate dehydrogenase and aspartate aminotransferase peaked 20-24 h later. The aim of this study was to evaluate the effect of heparin on these two-phases of enzyme release, using a pig model of hepatic ischemia-reperfusion injury. Twenty male swine were divided into control (n = 8) and heparin (n = 12) groups. In the heparin group, heparin was administered prior to and concurrent with ischemia-reperfusion. Following 45 min of hepatic ischemia, the levels of beta-galactosidase, beta-glucosidase, acid phosphatase, purine nucleoside phosphorylase, lipid peroxides, lactate dehydrogenase, and aspartate aminotransferase in serum were monitored for up to 166 h and compared to pre-ischemic and control levels. With heparin infusion, the peak levels of beta-galactosidase, beta-glucosidase, and the lipid peroxide were reduced to 50-60% of the control levels. Acid phosphatase and purine nucleoside phosphorylase activities in serum were reduced to 25% and 60%, respectively. The peak concentrations of lactate dehydrogenase and aspartate aminotransferase were reduced to about 25% of the control level. In addition, the serum enzymes of control pigs did not return to pre-ischemic levels until 2 weeks after hepatic ischemia, while they normalized in less than 1 week in the heparin-treated animals. Systemic heparinization had different protective effects on the first and secondary phases of liver injury. These differences may reflect heparin protection of different types of liver cells. The protection of the parenchymal cells may be the combined result of reduced sinusoidal cell injury and the anticoagulant properties of heparin.
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PMID:Differential effects of heparin on the early and late phases of hepatic ischemia and reperfusion injury in the pig. 1044 94

Phthalate esters have been implicated as xenoestrogens. One among them is di-ethylphthalate (DEP), which is used as plasticizer, detergent base, and binder in incense sticks and after-shave lotions. DEP is one of the contaminants of freshwater and marine ecosystems. Incense stick workers are occupationally exposed to DEP and some workers are chronic alcoholics. Therefore, a study was undertaken to evaluate the interactive toxicity of DEP with ethyl alcohol (EtOH) in young male Sprague-Dawley rats. The rats were given 50 ppm DEP (w/v), 5% EtOH (v/v) and a combined dose of 50 ppm DEP (w/v)+EtOH (5% v/v) in water ad libitum for a period of 120 days and were maintained on normal diet. Control animals received normal diet and plain water. During the treatment rats were weighed every week and water consumption per day was measured. After the completion of treatment, liver weight/body weight, liver weight, body weight, serum enzymes and other biochemical parameters were assessed. It was found that there was no significant change observed in body weight, liver weight, liver weight/body weight and water consumption. It was observed that there was a significant decrease in liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in EtOH, DEP and EtOH+DEP treated rats in the order of EtOH>DEP>EtOH+DEP as compared with control. Serum AST, ALT, acid phosphatase (ACP), alkaline phosphatase (ALP), succinate dehydrogenase (SDH) and liver ACP showed significant increase in DEP and EtOH+DEP treated rats in the order of DEP>EtOH+DEP as compared with control and EtOH treated rats. On the contrary, there was no significant change in liver ALP levels in treated rats. There was significant increase in liver SDH, glycogen, total triglyceride, total cholesterol and lipid peroxidation in DEP and EtOH+DEP treated rats, but no significant changes in the serum SDH, glucose and total triglyceride levels. Serum total cholesterol levels in DEP and EtOH+DEP treated rats were significantly high as compared to control and EtOH treated rats. These results show that there is no interaction of DEP with EtOH but DEP alone leads to severe impairment of lipid metabolism coupled with toxic injury to the liver as evident from significantly altered lipid and enzyme levels in the liver and serum. Long term simultaneous exposure to DEP and EtOH may have severe implications for humans who are occupationally exposed to these two xenobiotics.
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PMID:Simultaneous administration of diethylphthalate and ethyl alcohol and its toxicity in male Sprague-Dawley rats. 1083 29

Exposure of human plasma in vitro to gas-phase cigarette smoke (CS) causes a marked modification of plasma proteins as measured by protein carbonyl assay. Aldehydes present in CS may cause this elevation of protein carbonyls by reacting with sulfhydryl groups of proteins. Saliva is the first body fluid to confront the inhaled CS. Thus, in vitro exposure of saliva to nine "puffs" of CS also showed a distinct increase in protein carbonyls. Ascorbate and desferrioxamine mesylate had little effect on protein carbonyl formation, while GSH and N-acetylcysteine considerably inhibited the accumulation of protein carbonyls due to CS exposure. Following the exposure to CS, the activities of several salivary enzymes-amylase, lactic dehydrogenase (LDH), and acid phosphatase-were found to be significantly reduced (34, 57, and 77%, respectively). However, CS had no effect on the activities of aspartate aminotransferase and alkaline phosphatase. Addition of 1 mM of GSH and N-acetylcysteine considerably protected LDH and amylase activities, suggesting that sulfhydryl groups are affected in LDH and amylase. On the other hand, addition of 1 mM ascorbate caused a further loss of LDH and amylase activities, which could be partially prevented by the addition of desferrioxamine mesylate, implicating metal-catalyzed oxidation processes. Finally, loss of acid phosphatase activity was completely unaffected by any of the above antioxidants. It is concluded that the loss of salivary enzyme activities may be due to various agents in the CS that affect the enzyme activities via different mechanisms.
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PMID:Effect of cigarette smoke on salivary proteins and enzyme activities. 1089 39

In vitro study for the determination of the toxicity of some pesticides (glyphospate and paraquat) and cadmium chloride (CdCl2) on the activities of serum acetylcholinesterase (AChE), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), and acid phosphatase (AcP) is described. Changes in electrophoretic patterns of serum proteins were also tested. Results revealed that glyphosate was effective on all enzymes except AcP. Its IC50 values (the concentration of compound that inhibits 50% of the enzyme activity in 1 h at 37 degrees C) were 714.3, 750, 54.2, 270.8, and 71.4 mM for AChE, LDH, AST, ALT, and AlP, respectively. The inhibitory effect of paraquat varied markedly among all enzymes. The IC50 values of paraquat were 321.4 and 750 mM for AST and ALT, respectively. It had mild effect on AChE and LDH; and no effect on the activities of AlP and AcP. The effect of CdCl2 was pronounced with AChE, ALT, AlP, and AcP, and no effect on LDH and AST was found. The corresponding IC50 values were 77.7, 22.2, 33.3, and 83.3 mM for AChE, ALT, AlP, and AcP, respectively. Polyacrylamide gel electrophoretic patterns of serum proteins showed marked differences with glyphosate and CdCl2 but not with paraquat. The results suggest that the in vitro enzyme-activity test seems to have a potential for the assessment of pesticide and heavy metal toxicity.
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PMID:Influence of paraquat, glyphosate, and cadmium on the activity of some serum enzymes and protein electrophoretic behavior (in vitro). 1128 Dec 53

Attempts were made to detect and measure the activities of arylsulfatases. A&B acid phosphatase, lactate dehydrogenase, and glutamate oxaloacetate transaminase (aspartate transaminase) enzymes in human chronic lesions of endodontic origin. Thirteen periapical lesions of endodontic origin and 11 noninflamed control periapical tissues were obtained. The specimens were carried to the laboratory on liquid nitrogen and kept at -70 degrees C. Samples were thawed, homogenized, and then assayed for enzyme activities. The specific activities of arylsulfatase A (nmol/hr/mg protein) were 55.0+/-10.7 (chronic lesions) vs. 3.4+/-2.2 (controls) (p < 0.01). Arylsulfatase B specific activities (nmol/hr/mg protein) were 50.3+/-6.4 (chronic lesions) vs 91.8+/-18.4 (controls). Total acid phosphatase activities (mU/mg protein) were 45.8+/-6.6 (chronic lesions) vs. 26.8+/-3.1 (controls). Lactate dehydrogenase activities (Berger-Broida units/mg protein) of the chronic periapical lesions were significantly higher than the control group (362+/-63.2) vs. (140+/-46.0) (p < 0.05). There was no significant difference between the specific activities of aspartate transaminase in chronic lesions and the control group (68.0+/-14.5) vs. (53.0+/-10.4) mU/mg protein).
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PMID:Analysis of arylsulfatases A and B, acid phosphatase, lactate dehydrogenase, and aspartate transaminase in chronic periapical lesions of endodontic origin. 1148 69

Aphanamixis polystachya is a traditional medicinal plant of the Meliaceae family in India. A crude ethanolic extract of the leaf of this plant shows a beneficial effect on toxic liver injury. Its antihepatotoxic activity was evaluated on carbon tetrachloride (CCl4)-induced liver injury in a rat model. The assessment of hepatoprotective activity was evaluated by measuring the activities of aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), alkaline phosphatase (ALP), acid phosphatase (ACP) and lactate dehydrogenase (LDH), serum total bilirubin and albumin and histology of the liver. The crude leaf extract significantly inhibits the enhanced ASAT, ALAT, ALP, ACP and LDH activities released from the CCl4-intoxicated animals. It also ameliorated the depressed value of serum albumin and the enhanced value of total bilirubin in plasma caused by CCl4 intoxication. The study showed that the crude ethanolic extract from A. polystachya leaves provided protection against acute carbon tetrachloride-induced liver damage.
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PMID:Role of plant metabolites in toxic liver injury. 1189 Jun 39

Zinc (Zn) is an essential nutrient that is required in humans and animals for many physiological functions, including immune and antioxidant function, growth and reproduction. The present study was conducted to investigate the effects of adequate Zn level (38 mg/kg diet, as a control) and two low levels that create Zn deficiencies (19 mg/kg diet, 1/2 of the control and 3.8 mg/kg diet, 1/10 of the control) in growing male and female rats for 10 weeks. To evaluate the effects of these levels, the concentrations of thiobarbituric acid-reactive substances (TBARS), biochemical parameters and protein pattern were studied. Lipid peroxidation in liver, brain and testes of rats fed Zn-deficient diet was indicated by increased TBARS. Serum, liver, brain and testes glutathione S-transferase (GST) activities were significantly (P<0.05) increased in Zn-deficient rats, the effect was pronounced in rats fed the lowest level of Zn (1/10 of control). The activity of lactate dehydrogenase (LDH) was significantly (P<0.05) increased in liver, brain and testes, but decreased in serum in a dose-dependent manner. Zinc deficiency increased (P<0.05) liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in a dose-dependent manner, while there was no effect on the activity of these enzymes in testes. Zinc deficiency resulted in a significant (P<0.05) decrease in the activity of alkaline phosphatase (AlP) in serum and liver in a dose-dependent manner, but no effect in testes was found. The activity of acid phosphatase (AcP) was not affected in serum, liver and testes. Zn-deficient rats had higher liver concentrations of total lipids (TL), cholesterol, triglyceride (TG), and low density lipoprotein (LDL), while high density lipoprotein (HDL) was significantly (P<0.05) declined in a dose-dependent manner. Brain and serum acetylcholinesterase (AChE) activities were, however, not affected (P<0.05) by Zn deficiency. Protein content in liver, brain and testes showed a significant (P<0.05) decrease in rats fed the lowest level of Zn (1/10 of control). Polyacrylamide gel electrophoresis (native-PAGE) of serum proteins revealed that the intensity of immunoglobulins, serum albumin as well as several peptide bands were decreased in rats fed 1/2 or 1/10 of Zn adequate, i.e. their synthesis was affected and it was pronounced with the lowest level of Zn deficiency (1/10 of control). However, no clear effect on the transferrin was observed in both cases compared to controls. From the results of this study it can be concluded that Zn deficiency exerts numerous alterations in the studied biochemical parameters, protein pattern, and increased lipid peroxidation.
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PMID:Dietary zinc deficiency induced-changes in the activity of enzymes and the levels of free radicals, lipids and protein electrophoretic behavior in growing rats. 1204 50

The present study was undertaken to evaluate the dose-dependent effects of a leaf extract of Stephania hernandifolia on testicular activities in albino rats. Whether this leaf extract has any toxic effect on metabolic organs or on the liver or kidney was studied. Adult male Wistar rats, maintained under standard laboratory conditions, were forcefully fed with the aqueous extract of these leaves at the dose of 2 g or 4 g of leaves/mL distilled water/100 g body weight/day for 28 days. All the animals, along with vehicle-treated controls, were killed on the Day 29 of the experiment. Treatment with this leaf extract at both doses resulted in significant reduction in relative weight in the testis, the seminal vesicles, the prostate, and the epididymis without any significant change in the liver and kidney weight in comparison to control. Activities of testicular steroidogenic key enzymes and plasma testosterone level were decreased significantly, along with a significant reduction in the number of germ cells at stage VII of the spermatogenic cycle and in the seminiferous tubular diameter in both treated groups in comparison to control. Activities of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, acid phosphatase, and alkaline phosphatase were not altered significantly in the liver and kidney in both treated groups compared with controls. We concluded that treatment with an aqueous extract of leaves resulted in diminution in the activities of testicular androgenic key enzymes and plasma level of testosterone along with inhibition of spermatogenesis without any induction of hepatic and renal toxicity.
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PMID:Effects of leaf extract of Stephania hernandifolia on testicular gametogenesis and androgenesis in albino rats: a dose-dependent response study. 1205 93

Fifteen isolates of Verticillium dahliae (eight of race 1, seven of race 2; most from the island of Crete, Greece) were examined for isozyme and molecular variation. Among the isozyme banding patterns (zymograms) of six enzymes that were "activity-stained" after electrophoresis in 9% polyacrylamide gels, differences were observed in diaphorase, alpha-esterase, peroxidase and superoxide dismutase; 2, 2, 3 and 5 different types of zymograms were recorded, respectively. The zymograms could not be correlated with either race 1 or 2. However, all six isolates originating from the Oropedio (plateau) area of Lasithi (Crete) showed an esterase zymogram clearly distinguishable from the other isolates. No differences were observed when staining for acid phosphatase or aspartate aminotransferase ('glutamic-oxaloacetic transaminase'). Furthermore, electrophoresis of random-amplified polymorphic DNA (RAPD) in 2% agarose gels showed that three race-2 isolates from Oropedio of Lasithi could also be distinguished by the RAPD pattern generated with primer OPA-1. The variation observed possibly represents adaptation of V. dahliae to the Oropedio environment.
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PMID:Isozyme variation in Verticillium dahliae isolates from Crete. 1205 96

The efficacy of Tiron (4,5-dihydroxybenzene 1,3-disulfonic acid disodium salt) was examined in the treatment of beryllium-induced maternal and developmental toxicity in rats. Single administration of beryllium nitrate at a dose of 50 mg/kg (i.m.) on day 13 of gestation caused reductions in fetal and placental weights, the number of implantation sites and number of corpora lutea, as well as causing post-implantation loss, stunted growth, increase in the number of resorptions, and also a disturbed sex ratio. Maternal toxicity was demonstrated by reduction in body weight gain. Administration of beryllium also showed significant alteration in the hematological and biochemical indices of the mother as well as the fetus. Marked decreases were recorded in hemoglobin percentage, blood sugar levels, serum protein contents and serum alkaline phosphatase activity. By contrast, significant elevation was found in the activity of transaminases (aspartate aminotransferase and alanine aminotransferase). Tissue protein contents, glycogen contents, activities of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase of kidney, lungs and uterus, and maternal and fetal liver all showed significantly decreased values after beryllium exposure, and remarkable elevation was observed in acid phosphatase, glucose-6-phosphatase and hepatic lipid peroxidation. These parameters were restored considerably with administration of 471 mg/kg i.m. Tiron from days 14 to 18 of gestation. Atomic absorption spectrophotometry also revealed a high concentration of beryllium in different organs of pregnant rats. Interestingly, a small amount of metal ion was also detected in the fetus and reduced accumulation of beryllium was noticed after Tiron treatment.
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PMID:Protective effect of Tiron (4,5-dihydroxybenzene-1,3-disulfonic acid disodium salt) against beryllium-induced maternal and fetal toxicity in rats. 1218 11


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