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)

Protective effect of aprotinin pretreatment was assessed by functional, biochemical and morphological preservation in four hour global ischemia followed by one hour reperfusion in dogs. Cardioplegia was induced by intermittent infusion of cold Mg-lidocaine solution. Aprotinin 10,000 KIU/kg was given in low dose group (8 dogs), and 20,000 KIU/kg in high dose group (6 dogs); one half was given before ischemia and another half during ischemia. Betamethasone, coenzyme Q and nifedipine were also given equally in both groups before ischemia. Results were as follows: 1. Four (50%) of low dose group and all of high dose group were successfully taken off CPB and survived for one hour reperfusion. 2. High dose group showed significantly higher blood pressure and LVSWI than low dose group after one hour reperfusion (p less than 0.05). 3. Serum N-acetyl-beta-D-glucosaminidase and mitochondrial aspartate aminotransferase showed the significantly lower activity in high dose group than in low dose group after one hour reperfusion (p less than 0.05). There was no significant difference in the activities of serum beta-glucuronidase and MB-creatine kinase. 4. Myocardial tissues, excised after one hour reperfusion, contained significantly higher creatine phosphate in high dose group than in low dose group (p less than 0.05). There was no significant difference in the contents of adenosine triphosphate, calcium and water. 5. Severely injured mitochondrion were significantly lesser in high dose group than in low dose group. All lysosomes showed mild swelling or enlargement, but those membranous structures were well-preserved in both groups. In conclusion, aprotinin pretreatment might be effective in myocardial protection against prolonged global ischemia, by inhibiting the "leak out" of lysosomal enzymes.
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PMID:[Improved myocardial protection by aprotinin pretreatment in prolonged global ischemia]. 248 66

A group of 30 female albino rats were exposed to mosquito-coil smoke, 8 hours a day, 6 days per week, for 6 months. Another group which was exposed to air served as control. At the end of the experiment, the enzyme activities, total protein and lecithin contents as well as cellular responses in the lung lavage between the control and smoke-exposed rats were compared. Morphological observations using scanning and transmission electron microscopy demonstrated that the alveolar macrophages of smoke-exposed rats lost their typical ruffled membranes. They possessed small cytoplasmic processes on their smooth cell surfaces, small particles in phagolysosomes and mitochondria with a very electron-dense matrix. The levels of total protein and lecithin and the activities of lactate dehydrogenase, acid phosphatase and beta-glucuronidase in the lung-lavage fluid of smoke-exposed rats were significantly (P less than 0.05) higher than those of the controls. Increases (P less than 0.05) of serum enzymes, including lactate dehydrogenase, aspartate aminotransferase, isocitrate dehydrogenase and aldolase, indicated damage of liver tissues, but the levels of serum urea and urea nitrogen remained at the control levels implying normal functions of the kidneys of the mosquito-coil smoke-exposed rats. The level of serum tri-iodothyronine also increased significantly (P less than 0.05), but thyroxine remained at the control level.
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PMID:Biochemical and cellular changes in bronchoalveolar lavaged samples from rats after inhalation of mosquito-coil smoke. 256 17

Two methods of inducing liver cirrhosis in the rat were studied. Intragastric administration of CCl4 for 16 weeks according to Proctor and Chatamra was compared to the administration of thioacetamide in the drinking water (0.3 g/l) for the same period. CCl4 administration induced micronodular cirrhosis in 6/8 animals with a 27% mortality. Thioacetamide induced cirrhosis in 6/8 animals without mortality. The histologic pictures differed somewhat in that the CCl4 group exhibited more necrosis and cellular swelling while the thioacetamide group had more nuclear atypias and proliferation. Biochemically both groups had elevated plasma levels of aspartate aminotransferase. The lysosomal enzyme beta-hexosaminidase (beta-NAG) showed a transient increase in the thioacetamide animals, while beta-glucuronidase decreased. CCl4-induced cirrhosis led to an increase in beta-NAG. Plasma zinc decreased in both groups as well as liver zinc content in the CCl4 group, while there was a continuous elevation of liver zinc in the thioacetamide group. We conclude that oral administration of thioacetamide is a simple and reliable method of inducing experimental liver cirrhosis. The differences in histological appearances and some biochemical parameters may be caused by the different mechanisms of action of thioacetamide and CCl4.
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PMID:Thioacetamide- and carbon tetrachloride-induced liver cirrhosis. 276 88

Twelve serum analytes [triglycerides, cholesterol, total and conjugated bilirubin, high-density-lipoprotein cholesterol (HDL-C), alkaline phosphatase (AP), gammaglutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), beta-glucuronidase (beta-glu), alanine aminopeptidase (AAP), and 5'-nucleotidase (5'nuc)] were measured to investigate their correlation with exposure to polychlorinated biphenyls (PCBs) and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT). The relationship between serum lipids, lipophilic toxicants, and the analytes was also evaluated. The beta-glu, 5'nuc, triglycerides, cholesterol, and total bilirubin correlated positively and significantly with log concentrations of serum total PCBs and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), a metabolite of DDT. The more highly chlorinated PCBs (Aroclor 1260) had significant, positive correlations with several serum analytes, but the less chlorinated PCBs (Aroclor 1242) correlated significantly and negatively only with HDL-cholesterol. Triglyceride- and cholesterol-rich lipoproteins were added to serum to determine the effects of lipids on these assays. Several were spuriously elevated. AP and beta-glu were not affected by lipoprotein addition with the methods used in this study. AAP was increased significantly only at triglyceride concentrations exceeding 400 mg/dl. Lipoproteins may be elevated because of deranged lipid metabolism in response to PCBs, or PCBs may be elevated because elevated lipoproteins are present, as in familial triglyceridemia, a relatively common dyslipoproteinemia. Because this relationship is not well understood with respect to cause and effect, we propose the further use in epidemiological investigations of assay methods that are little affected by blood lipids yet are correlated with PCB concentrations. Congener-specific quantification of PCBs would help elucidate the effects of PCBs on assays used to monitor health effects.
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PMID:Effects of polychlorinated biphenyls and lipemia on serum analytes. 302 64

Plasma levels of the lysosomal enzymes, beta-hexosaminidase and beta-glucuronidase, were analyzed in rats with carbon tetrachloride induced liver cirrhosis. Out of 22 animals, 15 showed cirrhotic and 4 pre-cirrhotic livers. 4 cirrhotic animals exhibited cholestatic features with increased bilirubin, alkaline phosphatase (ALP) and aspartate aminotransferase (ASAT) in plasma. The remaining 15 pre-cirrhotic and cirrhotic rats showed clear significant changes only in ASAT levels. These 15 rats showed no consistent increase in plasma, spleen or liver lysosomal enzyme activities, whereas the 4 rats with cholestatic features exhibited considerable increases of lysosomal enzymes. The increased activities might be attributed to decreased biliary excretion and/or increased production of lysosomal enzymes by activated macrophages.
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PMID:Lysosomal enzymes in plasma, liver and spleen from rats with carbon tetrachloride-induced liver cirrhosis. 315 68

Guinea pig skin was treated with 50 mg/kg sodium lauryl sulphate (SLS) and nickel (Ni) alone and in combination (50 mg/kg SLS and 50 mg/kg Ni) for 7 and 14 days. Release of acid phosphatase, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, beta-glucuronidase, lactic dehydrogenase and malic dehydrogenase was observed, following treatment with SLS and Ni alone or in combination. Similarly, the skin contents of amino nitrogen and sulphydryl groups also increased significantly. These alterations were slightly more marked when the skin was treated simultaneously with the combination of SLS and Ni. The present study suggests that industrial workers or populations exposed simultaneously to SLS and Ni are more prone to dermal irritation or inflammation.
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PMID:Effect of sodium lauryl sulphate and nickel alone and in combination on the skin of guinea pigs. 317 54

Liver injury was induced by one subcutaneous administration of thioacetamide (200 mg/kg b.wt.) and studied 24 and 48 hrs later. Levels of aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) increased after 24 and 48 hrs. The lysosomal enzymes beta-hexosaminidase (beta-NAG) and beta-glucuronidase (beta-GLU) increased significantly after 24 hrs, while the level of beta-GLU returned to normal after 48 hrs, but the activity of beta-NAG remained significantly high even after 48 hrs. Histopathological examination showed necrotic hepatocytes around the central vein with infiltration of macrophages, neutrophils and eosinophils. The plasma zinc level decreased after 24 hrs and returned to normal after 48 hrs. Liver zinc content increased simultaneously at 24 hrs, returning to normal after 48 hrs. No alterations of plasma copper were observed after 24 and 48 hrs. Copper content of the liver increased significantly after 24 and 48 hrs. The present study thus shows that one dose of thioacetamide results in profound liver injury and supplementation of zinc prior to and simultaneously with thioacetamide normalized plasma zinc, increased liver zinc content and reduced the increase of beta-NAG, but did not influence the histological changes.
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PMID:Early biochemical and histological changes in rats exposed to a single injection of thioacetamide. 358 11

1. The rat uterus contains acid cathepsin, beta-glucuronidase, beta-galactosidase, acid phosphatase and deoxyribonuclease II at concentrations comparable with those found in liver. Two non-hydrolytic uterine enzymes, cytochrome c oxidase and aspartate aminotransferase, display only 2-6% of the activity found in liver. 2. The concentrations of acid cathepsin and beta-glucuronidase are significantly decreased in pregnancy and increase 3-4-fold during post-partum involution. 3. The concentrations of beta-galactosidase and acid phosphatase are not decreased in pregnancy and increase only 2-3-fold during involution. 4. The concentrations of these four acid hydrolases increase linearly during the first 4 days post partum and reach their peak values at the same time that wet weight and collagen content fall to their lowest point. 5. The concentration of deoxyribonuclease is depressed in pregnancy but does not rise above normal in the post-partum period. 6. Only a small proportion of each hydrolytic activity can be isolated in the mitochondrial-lysosomal fraction of sucrose homogenates of the rat uterus. This proportion increases during involution. However, the extensive mitochondrial rupture occurring during homogenization indicates that the technique is probably too harsh to obtain a true measure of the proportion of lysosomes present in the intact tissue. 7. There are no significant changes in either the concentration or subcellular distribution of the five acid hydrolases in the livers of the experimental rats during pregnancy or involution. In each case the largest proportion of the activity is found in the mitochondrial-lysosomal fraction of liver homogenates. 8. The results are interpreted in terms of the lysosomal theory of intracellular digestion.
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PMID:Acid hydrolases of the rat uterus in relation to pregnancy, post-partum involution and collagen breakdown. 589 45

Two regimens designed to ameliorate hepatic injury from complete liver dearterialization (LD) by interfering with lysosome-mediated proteolysis were studied in 200-g Buffalo rats. Five rats received a lysosome membrane-stabilizing flavenoid, catechin, 200 mg/kg/day for 5 days pre-LD. Five others were infused with lysosome protease inhibitors (LPI), leupeptin and pepstatin, delivered in 0.22-micron multilamellar liposomes at 500 micrograms each per hour for 2 hr, beginning 20 min before LD. Control groups (n = 4 or 5) were untreated LD, and treated and untreated sham LD rats. Blood from an arterial catheter pre-LD and 2 hr (peak enzyme release), 2 days, and 4 days post-LD yielded beta-glucuronidase (BG), aspartate transaminase (AST), and alkaline phosphatase values for each rat. Liver histology was not different between groups at 4 days post-LD. Untreated controls and the catechin LD group had similar enzyme levels at all points. LPI treatment values were statistically similar to sham LD values and had peak values significantly lower (P less than 0.05) than untreated LD controls at 2 hr. BG, 75 +/- 10 (SD) units per liter versus 185 +/- 32 units per liter; AST, 134 +/- 47 units per liter versus 459 +/- 175 units per liter. The BG lowering persisted to day 2 (55 +/- 25 units per liter versus 93 +/- 40 units per liter). Other values remained normal or normalized by Day 2. Hepatic damage as measured by enzyme release was not diminished by the membrane stabilizer catechin but was diminished after ischemic injury by specific targeted lysosomal protease inhibitors.
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PMID:Limiting ischemic liver injury by interfering with lysosomal autophagy. 685 23

Glutathion (GSH) plays an important role in maintenance of the redox state of the myocardium and acts as the membrane stabilizer. Seventeen patients who underwent cardiac surgery were subjected to cardiopulmonary bypass (CPB) and ischemic cardioplegia. The effect of GSH on ischemic myocardium was evaluated by serum lysosomal enzymes (acid phosphatase, beta-glucuronidase), isoenzymes of creatine phosphokinase (MB-CPK) and aspartate aminotransferase (m-GOT). standard CPB was instituted and systemic hypothermia was employed. GSH was administered to 8 patients in a dose of 200 mg/kg i.v. prior to institution of CPB. Mixed venous blood was sampled before administration of GSH, 10 min after institution of CPB and 0, 1, 6, 24 and 48 hr of reperfusion period following cardioplegia. Activity of acid phosphatase and beta-glucuronidase were significantly suppressed in the GSH-treated group compared to the non-treated group at 24 hours of reperfusion and immediately after aortic unclamping, respectively. Serum MB-CPK levels remained stable during reperfusion, but in the non-treated group, the level increased significantly at 6 hours of reperfusion. Increment of serum m-GOT levels was significantly suppressed at 1, 6 and 24 hours of reperfusion, compared to the non-treated group. These data suggest that pretreatment of GSH can protect the myocardium subjected to CPB from ischemic insult.
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PMID:Effect of glutathion pretreatment on hypothermic ischemic cardioplegia. 710 61


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