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

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

Pretreatment of rats with large doses of vitamin A (VA) potentiates the hepatotoxicity of CCl4. Because our previous studies indicate that VA treatment does not enhance CCl4 metabolism but does enhance CCl4-induced lipid peroxidation and activates liver Kupffer cells to release increased amounts of oxygen-centered free radicals, the current studies were designed to determine if VA treatment potentiates CCl4-induced liver injury through increased release of reactive oxygen species. Plasma clearance of colloidal carbon, an index of Kupffer cell phagocytic activity, was enhanced two- to threefold in rats treated for 7 days with VA (retinol, 250,000 IU/kg per day). Accordingly, VA treatment alone caused Kupffer cell activation. To determine if these activated Kupffer cells could potentiate hepatic injury through release of reactive oxygen species upon CCl4 challenge, polyethylene glycol coupled-superoxide dismutase (PEG-SOD, 10,000 IU/kg) or -catalase (PEG-CAT, 40,000 IU/kg) was given iv 2 hr after CCl4 (0.15 ml/kg, ip) to control or VA-pretreated rats to quench any released reactive oxygen. PEG-SOD and PEG-CAT effectively blocked VA potentiation of CCl4 liver injury as assessed at 24 hr by change in plasma ALT. Methylpalmitate (MP, 2 g/kg), an inhibitor of Kupffer cell phagocytosis and related oxygen burst, also blocked the potentiation of liver injury when given iv 24 hr before CCl4 to VA-pretreated rats. At the doses used, PEG-SOD or PEG-CAT did not influence CCl4 toxicity in control rats (at 0.15 or 2 ml CCl4/kg). Importantly, SOD, CAT, and MP blocked the enhanced lipid peroxidation induced by CCl4 in VA-pretreated rats. From these findings we conclude that the potentiation of CCl4 liver injury by VA pretreatment is mediated, at least in part, by active oxygen species released from Kupffer cells and possibly other macrophages that are activated by VA. Supporting this conclusion is the failure of VA pretreatment to increase the release of LDH from suspension of hepatocytes incubated with CCl4.
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PMID:Vitamin A potentiation of carbon tetrachloride hepatotoxicity: role of liver macrophages and active oxygen species. 848 Mar 39

The aim of this study was to determine whether antibodies to HCV can be hidden in immunocomplex aggregates in anti-hepatitis C virus (HCV) negative, HCV-RNA positive patients and whether their presence could be related to HCV viral load or HCV genotype. Sera (23 in toto) from patients with elevated alanine aminotransferase (ALT) levels and negative for anti-HCV but positive for HCV-RNA and the immunocomplex aggregates (precipitate with PEG 6000 and glycine 1 M) were studied. The sera were treated using a rapid, simple new ELISA which disrupted the immunocomplex aggregates. Sera from ten patients were tested anti-HCV positive after immunocomplex disruption. No correlation with age, sex, ALT level, viral load or HCV genotype was observed. In some patients anti-HCV antibodies were hidden in circulating antibody/antigen complexes which could be dissociated with a simple, inexpensive and rapid protocol; therefore it can provide a valuable addition to the diagnosis of HCV infection and it may prevent some cases of post-transfusion hepatitis.
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PMID:Anti-hepatitic C virus antibodies hidden in circulating antibody/antigen aggregates in HCV-RNA positive patients. 1103 47

This paper deals with the development of a technology for making a hydrophilic gel of polyethylene oxide reception in which radiating ability is employed to cause cross-linking of polymers in a water solution. The gel of polyethylene oxide was shown to be non-toxic, contain 5-50% of polymer and be useful in composite medicinal forms along with biologically active substances including Bac. subtilis proteases. Proteases immobilized in the gel possess high thermal stability and proteolytic activity and are readily applied in medicine. The effect of immobilized proteolytic and glucolytic enzymes of Bac. subtillis (Immozimase) on the warm ischemia-reperfusion (I/R) which can cause hepatic and jejunum injury was also studied. These enzymes were immobilized on water-soluble polymer polyethylene glycol by means of an electron beam. The number of degranulated mast cells as well as serum ALT after I/R in the group with Immozimase was decreased to almost half as compared with the control group. Pretreatment with Immozimase resulted in significant reduction of hepatic and gut neutrophil accumulation as compared with control animals. It was concluded that Immozimase has a protective effect for hepatic and gut ischemia/reperfusion, and this effect seems to be associated with prevention of leukocyte accumulation.
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PMID:Radiation technology in the preparation of polyethylene oxide hydrophilic gels and immobilization of proteases for use in medical practice. 1144 83

The addition of polyethylene glycol (PEG) to hepatocyte storage medium is known to decrease lipid peroxidation and swelling and to protect the cell cytoskeleton from cold. We therefore decided to investigate the effect of substituting PEG for hydroxyethyl starch (HES) in an extracellular-like UW solution, with and without Ca++, on rat liver preservation. Isolated perfused rat livers were used to assess graft injury after 24h of cold storage. Four groups of preserved livers ( n=6 for each group) were compared to controls (non preserved livers, n=11). For this purpose, Belzer solution (K+-UW, group 1) was stepwise modified. Group 2 (Na+-UW) was treated with the same liquid, however with inverted concentrations of Na+ and K+. Group 3 was preserved in the first experimental solution (EPS-1) with Ca++ (0.5mM) added to the Na+-UW solution. In the EPS-2 (group 4), PEG-35 (0.03mM) was substituted for HES. The last group, EPS-3 (group 5) was treated with the same compounds as EPS-2, but without Ca++. After 24h of cold storage and 120min normothermic reperfusion, there was no statistical difference in transaminases (ALT and AST) release between the control and the Na+-UW groups. Furthermore, rat livers preserved in Na+-UW solution released less ( P<0.05) ALT and AST and excreted more ( P<0.05) indocyanine green (ICG) than livers preserved in K+-UW solution. The addition of 0.5mM Ca++ to Na+-UW solution (EPS-1) dramatically increased ( P<0.05) parenchymal (ALT, AST) and non parenchymal (creatine kinase-BB) cellular injury. The substitution of PEG (0.03mM) for HES (EPS-2) reduced ( P<0.05) membrane injuries due to Ca++ while bile flow was statistically increased ( P<0.05). Finally, the omission of Ca++ from EPS-2, that is EPS-3, has no statistically significant effect on the studied parameters. PEG effectively protected the rat liver grafts from the onset of hypothermic ischemia-reperfusion and Ca++ damages and thus may be a valuable additive to preservation solutions.
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PMID:A preservation solution with polyethylene glycol and calcium: a possible multiorgan liquid. 1212 11

The joint injury actions and mechanisms of terephthalic acid (TPA), ethylene glycol (EG) and/or dowtherm A (DOW) on liver in rats were investigated. A subchronic toxicity study was designed by a 2(3) factorial method. Some enzymes, biochemical and morphologic indices reflecting the injury of liver were studied. The results showed that serum ALT and serum total bile acid (TBA) of rats in the combined intoxication groups were significantly higher than those in the groups with single toxic agent and control group. The results of factorial analysis showed that the joint action induced by TPA, EG and/or DOW were characterized as additive (TPA + EG), synergistic (EG + DOW), synergistic (TPA + DOW) and additive(TPA + EG + DOW) actions. The deduction was identified by morphologic observations.
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PMID:[Study on the injury of liver induced by terephthalic acid ethylene glycol and/or dowtherm A in rats]. 1256 62

An ad hoc committee appointed by the Italian Association for the Study of the Liver (AISF) proposed these Practice Guidelines for the management of HCV carriers with persistently normal aminotransferase levels. Only stringent ALT determinations will make it possible to distinguish these subjects from those in temporary biochemical remission. The overall prevalence in Italy has been estimated between 1.5 and 10.6%. HCV RNA quantitation and genotype determination are not predictors of the presence and severity of liver damage nor correlate with the outcome of the disease, and should not be used in clinical practice for the management and surveillance of HCV carriers with normal ALT. Only a minority of HCV carriers with normal ALT levels show a normal morphological picture (true 'healthy carriers'). Disease activity is mild in most cases; fibrosis is generally mild and cirrhosis is very rare. Histological activity, as monitored by sequential liver biopsies, seems to have very slow evolution. HCV carriers should not undergo liver biopsy on a routine basis. Liver biopsy can be reasonably proposed only in selected cases. Until the results of studies with PEG interferon plus ribavirin are available, HCV carriers should not receive antiviral treatment outside controlled experimental studies.
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PMID:Clinical management of HCV carriers with normal aminotransferase levels. 1284 10

Of the large number of patients chronically infected with hepatitis C virus (HCV), only about one third have progressive liver disease, and will eventually develop cirrhosis and hepatocellular carcinoma. These are the patients for whom effective antiviral treatment is most needed. Therapy is currently recommended for patients with chronic hepatitis C who have abnormal alanine aminotransferase (ALT) levels, detectable hepatitis C virus ribonucleic acid (HCV RNA) in the blood, and significant necroinflammatory changes and/or fibrosis on liver biopsy. The current gold standard in terms of treatment efficacy is the combination of peginterferon (PEG-IFN) and ribavirin. The overall sustained virological response rate (SVR) with these regimens is 54 to 61% following 48 weeks of therapy. Patients with genotype 1 infection have a 42 to 51% likelihood of response to 48 weeks of therapy. Those with genotypes 2 or 3 infection will respond to 24 weeks of therapy in 78 to 82% of cases. These SVR rates are 5 to 10 percentage points higher in all patient groups than in those obtained with standard doses of interferon (IFN) and ribavirin. Retreatment of nonresponders to standard IFN monotherapy using PEG-IFN and ribavirin has achieved SVR rates of 34 to 40%. Retreatment of patients who relapsed after IFN monotherapy has resulted in an SVR rate of about 60%. A SVR after retreatment of relapsers and nonresponders with PEG-IFN and ribavirin is more likely in patients previously treated with IFN monotherapy, those with HCV genotypes 2 or 3, patients with low viral load (<2 million copies/mL), and individuals who had a significant decrease in HCV RNA levels during the initial treatment. The potential benefits of long-term anti-HCV suppressive therapy in nonresponders are currently under investigation.
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PMID:Clinical trial results of peginterferons in combination with ribavirin. 1293 67

Combination therapy of PEG-IFN alpha-2a o alpha-2b plus ribavirin represents a further improvement in treatment of chronic hepatitis HCV+ with a sustained virological response (SVR) either in monotherapy (25-39%) either in association with ribavirin (59-56%). SVR is highly predictable: 75% of all patients who achieve viral clearance at week 12 (EVR), if they had an adherence > 80% of planned therapy, they become sustained viral responders. In spite of virological response, 16-34% of patients on PEG-IFN monotherapy have high value of ALT, and this make them to reduce adherence. 62 patients whith chronic hepatitis HCV+ and no corrhosis, have been treated for 48 weeks with PEG-IFN and ribavirin to evaluate discrepancy incidence between virological (HCVRNA < 200UI) and biochemical (normal value of ALT) response of patients treated with PEG-IFN plus ribavirin and to verify the impact that stuch discrepancy can produce on SVR of treated patients. Our preliminary data confirm that PEG-IFN bring a superior virological response than biochemical one, either on naive patients either on experienced ones even with ribavirin in association. It will be useful to verify if this discepancy cause a superior SVR as already reported by several studies. Even the follow-up of our 5 discordant patients confirm this trend.
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PMID:Discrepancy in virological and biochemistry response of patients with chronic hepatitis HCV positive on treatment with PEG-IFN plus ribavirin. 1451 25

Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies Knowledge Area of Prous Science Integrity(R), the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: 3,4-DAP; Adefovir dipivoxil, ADL-10-0101, alefacept, alemtuzumab, alosetron hydrochloride, ALT-711, aprepitant, atazanavir sulfate, atlizumab, atvogen; Bortezomib; CETP vaccine, clevudine, crofelemer; DAC:GLP-1, darbepoetin alfa, decitabine, drotrecogin alfa (activated), DX-9065a; E-7010, edodekin alfa, emivirine, emtricitabine, entecavir, erlosamide, erlotinib hydrochloride, everolimus, exenatide; Fondaparinux sodium, frovatriptan, fulvestrant; Gemtuzumab ozogamicin, gestodene; Homoharringtonine, human insulin; Imatinib mesylate, indiplon, indium 111 (111In) ibritumomab tiuxetan, inhaled insulin, insulin detemir, insulin glargine, ivabradine hydrochloride; Lanthanum carbonate, lapatinib, LAS-34475, levetiracetam, liraglutide, lumiracoxib; Maxacalcitol, melagatran, micafungin sodium; Natalizumab, NSC-640488; Oblimersen sodium; Parecoxib sodium, PEG-filgrastim, peginterferon alfa-2(a), peginterferon alfa-2b, pexelizumab, pimecrolimus, pleconaril, pramlintide acetate, pregabalin, prucalopride; rAHF-PFM, Ranelic acid distrontium salt, ranolazine, rDNA insulin, recombinant human soluble thrombomodulin, rhGM-CSF, roxifiban acetate, RSD-1235, rubitecan, ruboxistaurin mesilate hydrate; SC-51, squalamine; Tegaserod maleate, telbivudine, tesaglitazar, testosterone gel, tezosentan disodium, tipranavir; Vatalanib succinate; Ximelagatran; Yttrium 90 (90Y) ibritumomab tiuxetan; Zoledronic acid monohydrate.
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PMID:Gateways to clinical trials. 1467 84

Hot pepper (Capsicum annuum L. cv. Bugang) plants exhibit a hypersensitive response (HR) upon infection by Tobacco mosaic virus (TMV) pathotype P0. To elucidate molecular mechanism that underlies this resistance, hot pepper cv. Bugang leaves were inoculated with TMV-P0 and genes specifically up-regulated during the HR were isolated by differential screening. One of the clones, CaAlaAT1 encoding a putative alanine aminotransferase (EC 2.6.1.2) exhibited organ-specific expression pattern and the transcript accumulated abundantly in red (ripe) fruit tissues. CaAlaAT1 transcript was also induced in older leaves during senescence. The expression of CaAlaAT1 gene was increased in the incompatible interaction with TMV-P0 but was not in the compatible interaction with TMV-P1.2. When a strain of Xanthomonas campestris pv. vesicatoria (Xcv) carrying an AvrBs2 gene was infiltrated into the leaves of a pepper cv. ECW 20R carrying Bs2 resistance gene, a marked induction and maintenance of CaAlaAT1 gene expression was observed. The expression of CaAlaAT1 gene was triggered by salicylic acid (SA) and ethylene but not by methyl jasmonate (MeJA). CaAlaAT1 seemed to be localized mostly at the cytosol from the polyethylene glycol (PEG)-mediated transformation experiment. CaAlaAT1 seemed to catalyze alanine: 2-oxoglutarate aminotransferase (AKT) reaction, which was a main activity among the four activities in vitro, during the resistance response against TMV in hot pepper. These results suggest that CaAlaAT1, a protein known to be involved in metabolic reactions, might be one of the components in the plant's defense signal pathway against pathogens.
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PMID:CaAlaAT1 catalyzes the alanine: 2-oxoglutarate aminotransferase reaction during the resistance response against Tobacco mosaic virus in hot pepper. 1578 48


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