Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma components of 6 to 12-month-old beagles were examined using a Technicon auto-analyzer. Age-related changes were noted for 8 of the 21 components: the levels of total protein (T. Pro) and iron (Fe) gradually increased while those of alkaline phosphatase (ALP), creatine phosphokinase (CPK) and inorganic phosphorus (Pi) persistently decreased in both sexes. Triglyceride (Trigly) in female dogs, glutamic-pyruvic transaminase (GPT) and urea nitrogen (Urea-N) in male dogs tended to increase. The following thirteen components showed no significant variation during the period of observation: glucose (Glu), lactic dehydrogenase (LDH), albumin (Alb), creatinine (Crea), glutamic-oxaloacetic transaminase (GOT), leucine aminopeptidase (LAP), total bilirubin (T. Bil), amylase (Amy), total cholesterol (T. Chol), sodium (Na), potassium (K), chloride (Cl) and calcium (Ca). Our results generally agree with the reported findings on beagles from various institutions.
...
PMID:Plasma biochemistry values of young beagle dogs. 188 72

Iron-dependent oxy radicals have been implicated in reperfusion injury. Although the iron chelator desferoxamine (DFO) is beneficial, its hemodynamic effects and short vascular retention limit its use in vivo. We tested whether DFO conjugated to a high-molecular-weight starch might ameliorate in vivo hepatic microvascular injury without adverse side effects following 120 min of ischemia. Prior to reperfusion, conjugated DFO (100 mg/kg), vehicle (Veh), or saline (I/R) was administered. After 90 min of reperfusion, blood was collected for serum transaminase determination (ALT; U/liter), and fluorescein-albumin was injected to label perfused microvessels, which were quantified in frozen sections by a point-count technique. Tissue edema was estimated by wet to dry weight ratios (W/D). Reperfusion results in hepatocyte injury (rise in ALT and W/D) and a 30% loss of perfused microvessels. Intravenous administration of conjugated DFO produces no significant change in systemic hemodynamics, whereas both ALT and tissue edema were decreased by approximately 50%. Moreover, perfused microvessels were restored virtually to nonischemic control levels. Enhanced perfusion and attenuated cell injury with DFO suggest that microvascular failure and resultant cell death are mediated, at least in part, by iron-dependent mechanisms in reperfusion.
...
PMID:Conjugated desferoxamine attenuates hepatic microvascular injury following ischemia/reperfusion. 193 29

Hepatotoxicity of diethyldithiocarbamate (DDC) was investigated in rats. Plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were markedly elevated 24 hr after subcutaneous administration of DDC and histologically, the liver showed submassive necrosis. A sustained inhibition in the liver of Cu,Zn-superoxide dismutase (Cu-SOD) activity was observed following DDC treatment. DDC produced a significant loss in liver reduced glutathione (GSH) level after 1 hr, but the nadir was observed later than that of Cu-SOD. Catalase activity decreased gradually from 7 hr. Thiobarbituric acid reactive substances (TBARS) in the liver were significantly increased from 15 hr. Hepatic haemodynamics were scarcely changed up to 15 hr. Desferrioxamine (a chelator of iron) and piperonyl butoxide (an inhibitor of cytochrome P-450) prevented DDC-induced increases of both ALT and TBARS, but GSH did not, DDC hepatotoxicity was not changed by phenobarbital induction. Thus, we have shown that subcutaneous dose of DDC caused hepatotoxicity in rats. Although the exact sequence of its hepatotoxic factors is unproven, it seems likely that lipid peroxidation through the dysfunction of antioxidant defence factors and a toxic metabolite contribute to the formation of this liver injury.
...
PMID:Hepatotoxicity of diethyldithiocarbamate in rats. 196 45

Lipid peroxidation (LPO) and alterations in cellular systems protecting against oxidative damage were determined in the liver, kidney and skeletal muscle of male F344/NCr rats, 1 h to 3 days after a single intraperitoneal (i.p.) injection of 107 mumol nickel(II)acetate per kg body weight. At 3 h, when tissue nickel concentrations were highest, the following significant (at least, P less than 0.05) effects were observed: in kidney, increased LPO (by 43%), increased renal iron (by 24%), decreased catalase (CAT) and glutathione peroxidase (GSH-Px) activities (both by 15%), decreased glutathione (GSH) concentration (by 20%), decreased glutathione reductase (GSSG-R) activity (by 10%), and increased glutathione-S-transferase (GST) activity (by 44%); the activity of superoxide dismutase (SOD) and gamma-glutamyl transferase (GGT), as well as copper concentration, were not affected. In the liver, nickel effects included increased LPO (by 30%), decreased CAT and GSH-Px activities (both by 15%), decreased GSH level (by 33%), decreased GSSG-R activity (by 10%) and decreased GST activity (by 35%); SOD, GGT, copper, and iron remained unchanged. In muscle, nickel treatment decreased copper content (by 43%) and the SOD activity (by 30%) with no effects on other parameters. In blood, nickel had no effect on CAT and GSH-Px, but increased the activities of alanine-(ALT) and aspartate-(AST) transaminases to 330% and 240% of the background level, respectively. In conclusion, nickel treatment caused profound cell damage as indicated by increased LPO in liver and kidney and leakage of intracellular enzymes, ALT and AST to the blood. The time pattern of the resulting renal and hepatic LPO indicated a possible contribution to its magnitude from an increased concentration of nickel and concurrent inhibition of CAT, GSH-Px and GSSG-R, but not from increased iron or copper levels. The oxidative damage expressed as LPO was highest in the kidney and lowest in the muscle, which concurs with the corresponding ranking of nickel uptake by these tissues.
...
PMID:Nickel induced lipid peroxidation in the rat: correlation with nickel effect on antioxidant defense systems. 197 9

The induction heating to ferromagnetic implants (Ferromagnetic Induction Heating: FIH) has been developed for the purpose of selective hyperthermia on deep-seated tumors. In this investigation, the procedure of FIH combined with hepatic arterial embolization (HAE) was experimentally studied on VX2 liver tumor of rabbit. The induction heating unit is composed of radiofrequency generator (500 KHZ, 6-12 KW) and circular applicator (60 cm in diameter). Ferromagnetic implant used was pure iron particles (100 mu in size), which were suspended in tenacious polysaccharide solution to be injectable through a needle. After HAE with gelatin sponge powder had been made, iron particle suspension was injected into the cavity of tumor with subsequent exertion of induction heating (9KW) for 15 minutes. The measurement of temperature was made on the tumor and the liver parenchyma by fluoroptic thermometer with thin, flexible probe which readily passed through a needle. The temperature measured at peripheral area of tumor elevated at range from 2.5 to 7.1 degrees C, corresponding to the dose of iron particles injected; 2.5 degrees C with 1 g, 4.9 degrees C with 2 g, 7.1 degrees C with 3 g. In contrast, the temperature of liver parenchyma elevated at range of less than 2.5 degrees C, to indicate a successful selective heating of liver tumor. An additional experiment for the effect of heat on normal liver of rabbit were made using a microwave heating system. The histological and serologic examinations after heating of below 40 degrees C did not show any abnormal findings. After heating of 42-43 degrees C, however, serum GOT and GPT transiently elevated more than 3 times to that of before heating. Histologically, there were extensive degeneration and necrosis of liver tissue. From the results we concluded that FIH combined with HAE could provide an intensive therapeutic effect for treatment of well-localized liver tumors with minimal damages to the liver parenchyma, because of selective heating of the tumor.
...
PMID:[Experimental study of ferromagnetic induction heating combined with hepatic arterial embolization for treatment of liver tumors]. 208 99

The distributions of erythrocyte values (red cell count, hemoglobin concentration, etc.) of healthy male workers working in a certain factory were studied in order to evaluate the usefulness of the variables as health indicators. In addition to the estimation of erythrocyte values, anamneses concerning chronic bleeding, smoking habit and alcohol consumption were questioned and serum Fe, Cu, TIBC, ferritin, plasma erythropoietin, and serum enzymes (GOT, GPT, gamma-GTP) were measured. Two-dimensional frequency distributions with axes for the red cell count and hemoglobin concentration, and frequency distributions of the score calculated from principal component analysis, showed bimodal patterns. Using nonlinear curve fitting methods, the distributions of principal component scores were fitted to a mixture of two different Gaussian distributions. The workers were then divided into two groups corresponding to the Gaussian distribution he belongs. Then the frequencies of the items and mean values of the variates were compared between them. There were no differences in the incidences of diseases that caused iron deficiencies, but the mean serum ferritin level was significantly lower in one group than in the other, in other words the workers belonging to the group with low serum ferritin level had smaller iron stores than the other. The mean serum erythropoietin level and the mean serum copper level were higher in that group than in the other. As a result, this analysis gives a new evaluation of the health status of a man who belongs to the so-called healthy male group.
...
PMID:[Difference of iron stores represented in bimodal distribution of erythrocyte values among a healthy male group]. 221 98

The authors reported on a three month long EPREX (human recombinant erythropoietin) therapy of 5 hemodialysis patients for the treatment of their anemia. The drug was administered in bolus form 2 or 3 times a week after dialysis in a dose of 50 to 150 IU/bodyweight increased gradually in every (or every second) week. Hgb ad Htk values were determined once a week while erythrocyte, leukocyte, thrombocyte and reticulocyte count once a month. Serum iron, TIBC, serum ferritin, BUN, serum creatinine, urea, serum ions, liver function assays, serum lipids and amylase were also established. Hgb, Htk levels and reticulocyte count have significantly increased in the 4th week of treatment already, severe anemia ceased with improved appetite, general condition and physical strength. Serum urea and LDH levels significantly increased while SGOT decreased. No significant change in leukocyte and thrombocyte count, serum Na, K, Ca, P, Cl, BUN, creatinine, total protein level, serum albumin, bilirubin, alkaline phosphatase, GGT, GPT, amylase and blood sugar as well as serum lipid level were observed. No adverse reactions occurred during the treatment. After the three gradually decreased and within 6 weeks they had to be transfused again. In three patients the need for transfusion has significantly grown after the treatment. The authors consider EPREX a highly efficient drug in the treatment of anemia in dialysis patients.
...
PMID:[Recombinant human erythropoietin in the therapy of anemia in hemodialyzed patients]. 223 36

Treatment of rats with 100 mg kg-1 t-butyl hydroperoxide led to an enhanced ethane exhalation as a marker of in vivo lipid peroxidation, as well as a moderate hepatoxicity as evidenced by a rise in plasma activities of liver-specific enzymes (glutamate-pyruvate transaminase and sorbitol dehydrogenase) and an increase in hepatic calcium content. Furthermore, a depletion of hepatic glutathione by 17% was observed. Apart from the loss of glutathione, all these effects were antagonized by pretreatment of rats with the potent iron chelator deferrioxamine and potentiated by pretreatment with low concentrations of FeSO4 having no pro-oxidant activity per se; this was also the case in rats under conditions of iron overload (experimental haemochromatosis). These data indicate a close relationship between t-butyl hydroperoxide-induced lipid peroxidation and its hepatotoxicity, and point out the importance of iron in catalysing reinitiation (propagation) reactions of lipid peroxidation in vivo.
...
PMID:The role of iron in t-butyl hydroperoxide-induced lipid peroxidation and hepatotoxicity in rats. 225 81

The hepatotoxic and lipid peroxidative potentials of t-butyl hydroperoxide (t-BuOOH) towards isolated perfused rat livers were investigated at doses of 1 and 3 mmol l-1. t-BuOOH led to a concentration-dependent release of cytosolic (glutamate-pyruvate transaminase and lactate dehydrogenase) and mitochondrial (glutamate dehydrogenase) enzymes, an accumulation of calcium in the liver, a marked depletion of hepatic glutathione and an enhanced release of it into the perfusate, as well as an enhanced formation and release of malondialdehyde (MDA) by the liver. These effects were blocked in the presence of the potent iron chelator deferrioxamine, and enhanced in livers from iron-overloaded as well as in livers from glutathione-depleted rats. Our results indicate that the hepatotoxic and pro-oxidant actions of organic hydroperoxides depend upon the presence of ionized iron as a catalyst of radical-forming breakdown reactions, and are potentiated by impairment of glutathione-dependent detoxification reactions.
...
PMID:The role of iron and glutathione in t-butyl hydroperoxide-induced damage towards isolated perfused rat livers. 225 82

In a 106-wk toxicity and carcinogenicity study, groups of 60 male and 60 female weanling Wistar rats were fed 0, 0.5, or 50 mg bis(tri-n-butyltin)oxide (TBTO)/kg diet. In males, feed consumption was increased in all treated groups and increased water consumption occurred at 5 and 50 mg/kg. During the second year, body weight decreased in the 50-mg/kg males, while the females in that group showed no weight gain. Excess mortality was confined to the 50-mg/kg group towards the end of the study. Haematological changes, comprising anaemia, lymphocytopenia and thrombocytosis were noted mainly at the high-dose level. Also, signs of decreased kidney function and increased plasma enzyme activities (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) were noted. No effects on serum hormone concentrations (thyrotropin, follicle stimulating hormone, luteinizing hormone or insulin) were observed, except for a decrease in the free thyroxin:thyroxin ratio in both sexes at the high-dose level. Higher serum IgM and IgA levels were present at 50 mg/kg, while, in females, IgG was decreased. At 50 mg/kg, the ovaries, adrenals, spleen (females), heart (males), pituitary, liver and kidneys were increased in weight, but the thyroid weight was decreased in females. The total tin concentrations in liver and kidneys showed a dose relationship and, in general, the concentrations were similar after 1 and 2 yr. Non-neoplastic histological alterations after 1 yr consisted of a decrease in the cell height of the thyroid follicles in all dose groups, with a reduced number of psammoma bodies at 50 mg/kg, a decrease in splenic iron content at 5 (females only) and 50 mg/kg, and a slight bile-duct activation. After 2 yr, only the thyroid changes were still present. In addition, at 2 yr, vacuolation and pigmentation of the proximal tubular epithelium and nephrosis were enhanced at 50 mg/kg. The incidence of benign tumours of the pituitary was significantly elevated and enhanced at 0.5 and 50 mg/kg. At 50 mg/kg increases in pheochromocytomas in the adrenal medulla and in parathyroid adenomas (males) were noted, while adrenal cortical tumours were decreased (males). There was a low, non-dose-related incidence of pancreatic carcinoma. Other tumour rates were in line with control data. It is concluded that lifetime feeding of 50 mg TBTO/kg diet induces toxicity in various organ systems. An increase in some common tumours was found at the high dose, probably due to hormonal or immunological changes.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Chronic toxicity and carcinogenicity of bis(tri-n-butyltin)oxide (TBTO) in the rat. 234 92


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---