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)

Sixty-nine patients with chronic hepatitis C (CH-C) were treated with interferon therapy, and serum collagen type IV (s-collagen IV) levels were measured by enzyme immunoassay to analyze the responsiveness to interferon therapy. Classified by the improved pattern of serum alanine aminotransferase levels after interferon administration, 23 patients were judged as sustained responders, 23 as transient responders, and 23 as non-responders. Fibrotic grades of the liver sample correlated statistically with the levels of s-collagen IV (P < 0.01). Pre-therapy s-collagen IV levels of sustained responders were significantly lower than those of the other responders, and only sustained responders showed a significant decrease of s-collagen IV levels after interferon therapy, in accordance with histologic improvement. Multivariate analysis showed that s-collagen IV and hepatitis C virus genotype were the most important factors affecting the response to interferon therapy of all variates. Thus, s-collagen IV is one of the most useful aids for the evaluation of liver fibrotic grade in CH-C and a potent predicting indicator for the responsiveness to interferon therapy.
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PMID:Serum collagen type IV for the assessment of fibrosis and resistance to interferon therapy in chronic hepatitis C. 751 13

Liver injury produced by CCl4 depends on its metabolism by the liver cytochrome P450 enzyme system to a highly reactive intermediate (CCl3.). Cimetidine impairs cytochrome P450 and stimulates regenerative processes acting on DNA synthesis. This work was performed to investigate whether cimetidine may prevent CCl4-induced liver cirrhosis. Male Wistar rats were used: animals in group 1 received CCl4 (0.04 g per 100 g, i.p.) three times a week for 8 weeks; group 2 was treated with CCl4 plus cimetidine (120 mg kg-1, p.o.) three times a week for 8 weeks; group 3 received CCl4 for 8 weeks and then cimetidine for 4 weeks. Alkaline phosphatase, gamma-glutamyl transpeptidase (gamma-GTP) and alanine aminotransferase (ALT) activities, as well as protein and bilirubin, were measured in serum; collagen and lipoperoxidation were quantified in liver. Intoxication with CCl4 increased (P < 0.05) serum activities of alkaline phosphatase, gamma-GTP and ALT, and bilirubin concentration; liver collagen and lipoperoxidation were also increased. Cimetidine treatment prevented or reverted the increases in the three enzyme activities and in bilirubin content and the fall in proteins. It is worth noting that cimetidine co-treatment completely prevented both the increase in collagen content and the lipid peroxidation. The protective effect of cimetidine can be attributed to a reduction in cytochrome P450. However, it could also stimulate regenerative processes.
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PMID:Cimetidine prevents and partially reverses CCl4-induced liver cirrhosis. 791 3

Administration of alpha-naphthylisothiocyanate (ANIT) to rats results in periportal cholangiolitic hepatopathy. Inflammation is a hallmark of the liver injury, and expression of toxicity is dependent on blood neutrophils. The role of other cellular mediators of inflammation in ANIT-induced hepatic insult is unknown. We hypothesized that platelets participate in the expression of ANIT hepatotoxicity. To test this, circulating platelets were decreased by administration of anti-rat platelet serum (PAb) prior to treatment of rats with ANIT. The PAb treatment regimen effectively reduced circulating thrombocytes over the course of the experiment. Twenty-four hours after oral ANIT administration, rats were euthanized and liver injury was estimated by increases in serum alanine aminotransferase (ALT) and gamma-glutamyltransferase (GGT) activities. Cholestasis was assessed by measurement of serum total bilirubin concentration and bile flow. Reduction in platelet numbers was associated with attenuation of the increases in plasma ALT activity and bilirubin concentration seen after ANIT administration. However, PAb treatment did not attenuate the increase in plasma GGT, a marker of biliary epithelial cell injury. ANIT-induced changes in platelet function were assessed by evaluating platelet aggregation responses in platelet-rich plasma from rats treated with ANIT in vivo. ANIT treatment modestly decreased ex vivo platelet aggregation in response to ADP and collagen stimuli. To address further the role of platelet-derived cyclooxygenase products in ANIT hepatotoxicity, rats were treated with aspirin or ibuprofen. Neither pretreatment ameliorated ANIT-induced hepatic insult. These results suggest that platelets contribute to the expression of ANIT-induced liver injury, but they do not appear to act through the production of cyclooxygenase metabolites.
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PMID:Platelets and alpha-naphthylisothiocyanate-induced liver injury. 799 11

Massive hepatic cell necrosis can be induced by Corynebacterium parvum and lipopolysaccharide (LPS) in rats. In this model, serum LDH, GOT and GPT activities are significantly increased in vivo within several hours after LPS injection. An in vitro experimental acute liver injury animal model was produced by using multicellular spheroids composed of rat parenchymal and non-parenchymal liver cells. These multicellular spheroids were prepared by detaching the confluent monolayer on the collagen-conjugated thermo-responsive polymer coated culture dish at a temperature below the lower critical solution temperature and culturing it on the non-adhesive substratum. LPS caused clear elevations of GOT, GPT and LDH activities from these spheroids into the medium. However, the increase of LDH activity was only observed in the monolayer culture system. These results suggest that the multicellular spheroids of liver cells are useful models as an alternative to animal tests for hepatotoxicity.
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PMID:An experimental model of acute liver injury using multicellular spheroids composed of rat parenchymal and non-parenchymal liver cells. 812 32

Serum levels of the tissue inhibitor of metalloproteinases-1 (TIMP-1) were measured in 268 patients with liver diseases by means of a one-step sandwich enzyme immunoassay. In the cases of acute hepatitis, chronic active hepatitis (CAH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC), the levels of TIMP-1 were higher than those of the control group. Tissue inhibitor of metalloproteinases-1 levels correlated with type III procollagen peptide and with type IV collagen, indicating TIMP-1 as a useful marker for hepatic fibrosis. Levels of TIMP-1 also correlated with aspartate aminotransferase and alanine aminotransferase levels and showed the highest levels in acute hepatitis. Thus, TIMP-1 might also reflect hepatic inflammation. Serum levels of alpha-fetoprotein and TIMP-1 had a significant positive correlation in patients with HCC. A cut-off level of TIMP-1 between LC and HCC was set at 440 ng/mL, having a low sensitivity and a high specificity. These results suggest the usefulness of TIMP-1 as a tumour marker in cases of HCC where alpha-fetoprotein levels are not elevated.
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PMID:Clinical evaluation of serum tissue inhibitor of metalloproteinases-1 levels in patients with liver diseases. 821 91

Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are major proinflammatory cytokines inducing the synthesis and release of many inflammatory mediators. They are involved in immune regulation, autoimmune diseases, and inflammation. Acanthoic acid, (-)-pimara-9(11),15-dien-19-oic acid, is a pimaradiene diterpene isolated from the Korean medicinal plant, Acanthopanax koreanum. When human monocytes/macrophages stimulated with silica were treated with 0.1-10 microg/ml acanthoic acid, the production of IL-1 and TNF-alpha was inhibited up to 90%, but the production of interleukin-6 (IL-6) was not inhibited at all. At these concentrations, it had no cytotoxic effect on human monocytes/macrophages. It also suppressed the production of TNF-alpha by alveolar macrophages and lymphocytes stimulated with silica. In addition, acanthoic acid inhibited the release of superoxide anion and hydrogen peroxide from human monocytes/macrophages and neutrophils. To know the antifibrotic effects of acanthoic acid, its effects on fibroblast proliferation and collagen synthesis were tested. The proliferation of NIH3T3 cells was inhibited almost completely by the addition of the culture supernatants of human monocytes/macrophages treated with acanthoic acid, but not by the addition of acanthoic acid only. In vitro and in vivo treatment with acanthoic acid reduced collagen production by rat lung fibroblasts and lung tissue. Furthermore, acanthoic acid suppressed granuloma formation and fibrosis in the experimental silicosis. Acanthoic acid reduced serum GOT and GPT in the rats with cirrhosis induced by CCl4, and it was effective in reducing hepatic fibrosis and nodular formation. Taken together, these data indicate that acanthoic acid has a potent anti-inflammatory and antifibrosis effect by reducing IL-1 and TNF-alpha production.
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PMID:Suppression of interleukin-1 and tumor necrosis factor-alpha production by acanthoic acid, (-)-pimara-9(11),15-dien-19-oic acid, and it antifibrotic effects in vivo. 866 Aug 20

We examined 95 ground squirrels to compare the histological appearance of liver sections from animals that were chronically infected with ground squirrel hepatitis virus (GSHV) (n = 29), uninfected (n = 42), or had recovered from infection (n = 24). We studied the effects of long-term infection because these animals had been infected with GSHV for up to 10 years. Chronic infection generally produced a mild, persistent hepatitis characterized by light lymphocytic and plasmacytic portal infiltrates with occasional individual necrotic hepatocytes and small aggregates of Kupffer cells or mononuclear inflammatory cells in the parenchyma. In a few of the portal tracts from each of the more inflamed livers (grade 2), the inflammatory infiltrate penetrated the limiting plate and extended into the adjacent parenchyma. Hepatitis (grades 1 or 2) was detected more often in chronically infected animals (17 of 29) than in recovered (4 of 24) or uninfected ground squirrels (7 of 42). Fibrosis was generally not increased, but fine strands of collagen extended from the portal tracts and central veins into the parenchyma of about one quarter of the infected and recovered animals. Cytoplasmic pigment accumulation and variation in the size of hepatocyte nuclei appeared to be related to aging, not infection. Serum levels of aspartate and alanine transaminases (AST and ALT) were mildly elevated in samples from seven infected animals compared with seven control animals. Despite many years of chronic infection, liver injury was similar to that reported in previous studies on animals infected for shorter intervals, indicating that liver injury is not progressive in GSHV-infected ground squirrels.
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PMID:Non-neoplastic liver disease associated with chronic ground squirrel hepatitis virus infection. 867 46

Argon laser trabeculoplasty (ALT; 1.0 W, 0.1 sec, 50 microns) was performed in right eyes, and low energy, Q-switched Nd:YAG laser trabeculoplasty (Nd:YAGLT; 1.1-4.8 mJ/pulse) in left eyes of 14 patients with primary open-angle glaucoma and in one patient with juvenile glaucoma. The pre-laser intraocular pressure (IOP) was medically uncontrollable (IOP > 21 mmHg). The interocular pressure difference varied between 0 and 3 mmHg. In 9 patients IOP decreased to less than 22 mmHg (success) in both eyes. No statistically significant difference has been revealed with paired t-test in the degree of IOP decrease between ALT and Nd:YAGLT treated eyes during the 1-18 months' follow-up. Treatment variables of Nd:YAGLT had no statistically significant effect on the duration of the post-laser success with Cox-regression. In 4 patients both treatments were ineffective (IOP > 21 mmHg). In 2 patients ALT was successful but Nd:YAGLT was ineffective. In three cases of early bilateral laser failure (IOP > 21 mmHg at the first month visit) trabeculectomy was performed on both eyes in the third post-laser month. Following ALT the uveoscleral meshwork was severely destroyed in the area of the laser spots, and the surrounding collagen fibres were heat-damaged. The meshwork between the laser spots was covered by a membrane formed by migrating endothelial cells. In the uveoscleral meshwork Nd:YAGLT induced severe focal damage surrounded by circumscript shrinkage and scarring. The juxtacanalicular tissue remained free of laser induced damage. No endothelial membrane was present. The results suggest that low energy, Q-switched Nd:YAGLT may represent an alternative method of glaucoma laser surgery.
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PMID:Argon and low energy, pulsed Nd:YAG laser trabeculoplasty. A prospective, comparative clinical and morphological study. 873 75

In order to elucidate the clinical significance of serum hyaluronan in chronic viral hepatitis, serum hyaluronan concentrations were measured using a sandwich enzyme binding assay in 115 patients with chronic viral hepatitis. These findings were examined in relation to the results of laboratory liver tests, levels of serum markers for fibrosis and liver histological findings. Serum hyaluronan levels increased with the progress of liver disease, particularly in liver cirrhosis. There were no significant differences in serum hyaluronan levels among the cirrhotic patients according to Child's grade. Multivariate analysis showed that the significant independent predictors of serum hyaluronan were serum aspartate aminotransferase (P = 0.020), serum alanine aminotransferase (P = 0.008), serum cholinesterase (P < 0.001), particularly serum type IV collagen 7S domain (P < 0.0001), and the histological degree of liver fibrosis (P < 0.0001). These findings suggest that elevated serum hyaluronan levels are closely related to the severity of liver fibrosis. We assessed the predictive value of serum hyaluronan in differentiating cirrhosis from chronic hepatitis, constructing receiver operating curves; we found that serum hyaluronan was a better test for diagnosing cirrhosis than serum type IV collagen 7S domain and laboratory liver tests.
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PMID:Clinical significance of serum hyaluronan in patients with chronic viral liver disease. 874 18

Liver fibrosis was induced by chronically (7 weeks) administering CCl4 to rats. Animals were divided into four groups: (a) controls, (b) treated with CCl4 alone, (c) treated with CCl4 and colchicine and (d) treated with CCl4 and formyl-colchicine bound to lactosaminated serum albumin (FC-LASA). Liver dysfunction was monitored by biochemical tests (alkaline phosphatase [ALP], gamma-glutamyltransferase [gamma GT], aspartate and alanine transaminases [AST and ALT], albumin and total bilirubin). Fibrosis was evaluated by determining hydroxyproline and by microscopic examination. The exposure to CCl4 produced major alterations of liver structure and collagen deposition. These effects were partially counteracted by colchicine and to a greater extent by FC-LASA. Morphological findings paralleled biochemical data. The information reported here indicates that colchicine has an antifibrotic activity on the liver of intoxicated rats and that FC-LASA is more active than colchicine itself as an antifibrotic agent.
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PMID:Formylcolchicine bound to lactosaminated serum albumin is a more active antifibrotic agent than free colchicine. 889 3


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