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:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunohistochemical evaluation of Cu, Zn- and Mn-superoxide dismutase (SOD) activity in various viral liver diseases was performed by the peroxidase-conjugated antibody indirect method. Anti-human Cu, Zn-SOD (rabbit) and anti-human Mn-SOD (guinea-pig) derived and purified from SOD of human erythrocytes and placentas were used to determine SOD distribution in liver tissues. SOD in the liver tissues was detected in 68 inpatients of our unit. They consisted of 23 cases with chronic hepatitis caused by hepatitis B virus (13) and hepatitis C virus (10), 24 with liver cirrhosis caused by hepatitis B virus (5) and hepatitis C virus (19) (15: compensatory, 9: decompensatory) and 21 with hepatocellular carcinoma caused by hepatitis B virus (2) and hepatitis C virus (18) complicated of liver cirrhosis. In viral liver diseases, SODs in the liver tissues were distributed to hepatocytes mainly in the pattern of cytoplasmic diffusion. The incidence of immunohistochemical Cu, Zn-SOD and Mn-SOD were 47.8% and 56.5% in chronic hepatitis, 93.3% and 86.7% in compensated liver cirrhosis, 11.1% and 22.2% in decompensated liver cirrhosis, respectively. The aggression of viral liver disease was accompanied with the decrease of SOD concentration in the liver tissues. Hepatocellular carcinoma cells were negative for Mn-SOD in all cases, and weakly positive for Cu, Zn-SOD in 2 out of 21 cases. Comparatively strongly positive SOD findings were obtained from normal regions neighboring carcinomas. A close relationship between the depletion of SOD in liver tissues and carcinogenesis in viral liver diseases was observed.
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PMID:Relationship between superoxide dismutase (SOD) and viral liver diseases. 132 May 79

The association of HBV infection and glomerular damage was first reported by Combes et al in 1971, in a patient with nephrotic syndrome due to membranous glomerulopathy and chronic hepatitis B. Since, then, other glomerular diseases have been reported such as a) minimal changes nephropathy, b) IgA nephropathy, c) membranous-proliferative glomerulonephritis (MPGN), d) membranous, e) mesangial proliferative and f) lupus nephritis. All of them are associated with chronic hepatic disease and some of the following antigens: 1) HBsAg; 2) HBeAg; 3) HBcAg. These disorders are very frequent in Southeast Asia. Vertical transmission from mothers to fetuses may be important in maintaining the high carrier rate, and possibly plays a role in the development of glomerular damage. On the other hand, MPGN associated with HBsAg has rarely been reported and always with a favorable benign course. The present report describes interesting findings in a renal biopsy from a HBsAg and HBeAg carrier, who developed renal failure requiring hemodialysis. A 21 year old Korean man was admitted to the Hospital for nephrotic syndrome, microhematuria hypertension and renal failure. He had no previous history of blood transfusion, intravenous drug addiction, jaundice or liver disease. His father was HBsAg carrier with hepatic cirrhosis. An ultrasound examination showed normal renal size. Renal biopsy was performed and the patient received hemodialysis treatment. The specimen was processed for light microscopy, immunofluorescent studies and peroxidase-antiperoxidase technique. Frozen sections were studied by direct immunofluorescence for the identification of IgG, IgA, C1q, C3, fibrinogen and albumin. Paraffin sections stained by immunoperoxidase technique for HBsAg, using polyclonal monospecific rabbit anti-Human antisera (Dakopatts, Copenhagen).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Membranoproliferative glomerulonephritis with semilunar forms and massive deposits of IgA associated with HBsAg]. 229 14

The purpose of this paper is to provide a histopathologic basis for abnormalities in immune-complex clearance in liver disease. Fc receptors in CCl4-induced liver cirrhosis in rats were studied by applying peroxidase-antiperoxidase immunoglobulin G complex as a ligand to the frozen sections. Intravenous injection of bovine serum albumin-antibovine serum albumin complexes or colloidal carbon was combined with histological staining for endogenous peroxidase, fibronectin, laminin, or a lectin, Bandeiraea simplicifolia agglutinin I. In the cirrhotic process, sinusoidal Fc receptors showed a weakened reactivity to the ligand with focal absence, and the length of the Fc receptor-positive portion of the sinusoids in unit area decreased to about 50% of the normal value in the advanced cirrhosis. Fibronectin and the lectin showed the presence of sinusoids where Fc receptors were absent. The endothelium in Fc receptor-negative areas did not take up either immune complexes or carbon, and Kupffer cells were absent in these areas. A disturbed immune-complex metabolism was thus suggested to occur in association with the defect of sinusoidal Fc receptors in liver cirrhosis. These abnormalities appeared to not be directly related to perisinusoidal laminin deposition, i.e., capillarization of the sinusoid.
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PMID:Defect of sinusoidal Fc receptors and immune complex uptake in CCl4-induced liver cirrhosis in rats. 234 26

Aggregation and derangement of cytokeratin intermediate filaments are thought to be the key mechanism in the formation of Mallory bodies in alcoholic liver disease (ALD). To study the incidence and patterns of intracellular distribution of aggregated cytokeratin and to determine its utility as a diagnostic marker of ALD, 108 liver biopsy specimens from patients with various liver abnormalities were examined by an avidin--biotin peroxidase complex technique on paraffin section using a monoclonal antibody to cytokeratins (Hybritech). In normal liver (n = 11), only bile duct epithelium was positive. Both bile ducts and hepatocytes were positive in pathologic livers (n = 97). In ALD, 82 per cent of cases (42 of 51) showed cytokeratin positivity versus 15 per cent (seven of 46) in nonalcoholic liver disease (e.g., chronic hepatitis, nonalcoholic cirrhosis, cholestasis, and primary biliary cirrhosis). The highest incidence (100 per cent, 37 of 37) of positivity was obtained in cases with alcoholic hepatitis and cirrhosis compared with only 36 per cent (five of 14) in alcoholic fatty liver. Mallory bodies were found by the immunoperoxidase method in 71 per cent of cases (30 of 42) versus in 40 per cent (17 cases) by hematoxylin--eosin stain. In alcoholic fatty liver and alcoholic hepatitis, centrilobular hepatocytes showed cytokeratin positivity, whereas such reactivity was seen predominantly at the periphery of the regenerative nodules in alcoholic cirrhosis. A rare periportal hepatocyte was positive in the nonalcoholic group. These findings suggest that the differential distribution patterns of aggregated cytokeratin may be helpful in differentiating alcoholic from nonalcoholic liver diseases.
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PMID:Distribution patterns of cytokeratin antigen determinants in alcoholic and nonalcoholic liver diseases. 243 6

A sensitive procedure involving lectin affinity electrophoresis of alpha-fetoprotein (AFP) was established. AFPs electrophoresed on lectin-containing gels were blotted on nitrocellulose membrane which was precoated with the specific antibody to AFP and stained with peroxidase-labeled anti-AFP antibody. This method could detect as little as 4 micrograms/l of purified AFP dissolved in buffer, or 50 micrograms/l in serum specimens. A number of patients with liver disease have been followed for long periods in Nihon University Hospital, Tokyo. Serum specimens were collected serially and stored frozen. We have reinvestigated retrospectively 6 series of serum specimens by the lectin-immunoblotting technique and found 3 cases that revealed a hepatocellular carcinoma-specific AFP variant at a very early stage, in advance of any other evidence of hepatocellular carcinoma by clinical examination.
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PMID:Early diagnosis of hepatocellular carcinoma with lectin electrophoresis of serum alpha-fetoprotein. 245 97

The clinical and histologic significance of cytokeratin antigen expression in various intrahepatic locations was assessed in 57 patients with alcoholic liver disease as part of a large Veterans Administration Cooperative Study of Alcoholic Hepatitis. Cytokeratin antigen was demonstrated in fixed, paraffin-embedded liver tissue by an avidin-biotin peroxidase method using a mixture of two different monoclonal antibodies, AE1 (acidic; 48, 50 and 56.5 kD) and AE3 (basic; 52, 56, 58 and 65 to 67 kD). In contrast to the normal liver, in which only bile duct epithelium was positive, this antibody mixture stained both bile ducts and hepatocytes in pathologic livers. Serum levels of vitamin A showed a significant inverse correlation with the amount of cytokeratin antigen (scale: 0 to 3) in hepatocytes without Mallory bodies (p = 0.001), in Mallory body-containing hepatocytes (p less than 0.0001) and in bile ducts (p = 0.0074). Increased amount of cytokeratin antigen in each of these locations, in turn, correlated directly with the histologic severity of the liver disease. Histologic severity (fibrosis, parenchymal degeneration/necrosis, hepatocyte regeneration and inflammation) was significantly higher in patients when either Mallory bodies (p less than 0.0001) or cytokeratin antigen (p = 0.0021) was present in hepatocytes. Demonstration of cytokeratin antigen in hepatocytes which contained Mallory bodies correlated positively (p = 0.03) with clinical severity of the liver disease as determined by high serum bilirubin and prolonged prothrombin time (Maddrey's discriminant function).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum vitamin A deficiency and increased intrahepatic expression of cytokeratin antigen in alcoholic liver disease. 245 8

In an attempt to clarify the Kupffer cell function in alcoholism, chronic ethanol-fed rats were investigated. The clearance of latex particles in the rat was analysed to estimate the function of the reticuloendothelial system in the liver, and the phagocytic function of Kupffer cells was measured by counting particles in the cell after isolation of non-parenchymal cells by collagenase digestion of the liver following an injection of latex particles and subsequently by staining of endogenous peroxidase activities. In addition, the number of Kupffer cells and their phagocytic function were examined histologically in fresh frozen sections of liver after an injection of particles. Serum ethanol concentration in the ethanol-fed rats was 10-60 mumol/l. The clearance of latex particles was markedly reduced in the ethanol-fed rats as compared with the paired controls (P less than 0.01). Markedly decreased-phagocytic function was found in 20% of Kupffer cells in the chronic ethanol-fed rats. The number of Kupffer cells in the ethanol-fed rats was increased as compared with the paired control rats. Chemotaxis analysis revealed that hepatocytes when incubated with ethanol, produced chemotactic factor for Kupffer cells and polymorphonuclear cells. These abnormal Kupffer cell functions may contribute to the pathogenesis of alcoholic liver disease.
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PMID:Kupffer cell function in chronic ethanol-fed rats. 269 94

Liver biopsy specimens from patients positive for serum HBsAg reveal various expression patterns when properly stained by immunohistochemical techniques for the demonstration of HBsAg, HBcAg and HDAg. A negative staining for these three antigens seems to be associated with two conditions, i.e., self-limiting acute lobular hepatitis (ALH) or low amounts of intrahepatic antigens. The discrepancy between serum positivity and tissue negativity for HBsAg can be explained either by sampling error or by the higher sensitivity of the radioimmunoassay as compared with immunohistochemical methods. The use of amplification systems such as the avidin-biotin-peroxidase complex enhances the sensitivity of immunohistochemical peroxidase-antiperoxidase (PAP) techniques and makes it possible to detect very small amounts of both HBsAg and HBcAg in liver cells from paraffin-embedded tissue sections which had been negative with the conventional PAP technique. In cases with a positive staining for viral antigens, two main expression patterns (non-aggressive and aggressive) can be distinguished. The non-aggressive pattern is reflected in the HBcAg-free HBsAg-positive type (HBsAg carrier) or the generalized type of nuclear core (HBcAg carrier), while the aggressive pattern is reflected in the presence of HDAg, the presence of HDAg and HBcAg, the focal type of nuclear core or the cytoplasmic HBcAg. Superinfection of HBsAg carriers or switching from generalized to focal core, with or without cytoplasmic expression of HBcAg, results in transition from non-aggressive to aggressive pattern. The aggressive pattern occurs in association with histological features of chronic active hepatitis (CAH). When it occurs in ALH cases or in milder forms of chronic hepatitis, an evolution into CAH has to be expected. Features of severe CAH, eventually with cirrhosis, are found in association with two new expression patterns: the cytoplasmic core and the simultaneous presence of HBcAg and HDAg. When features of CAH are observed in liver tissue specimens with HBcAg-free HBsAg-positive type, the liver disease may be due to viral superinfection or to non-viral etiology, e.g., alpha 1-antitrypsin deficiency.
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PMID:Immunohistochemical techniques for the demonstration of viral antigens in liver tissue. 306 47

Liver biopsy specimens from 58 American patients with chronic type B hepatitis were investigated for the presence and distribution of the hepatitis B core (HBcAg) and surface (HBsAg) antigens by peroxidase-anti-peroxidase techniques. HBsAg was detected in 43 (77%) and HBcAg in 52 (90%) patients. HBcAg was present in 50 of 51 (98%) patients with hepatitis B e antigen (HBeAg) but in only two of seven (29%) of patients with antibody to HBeAg (anti-HBe). There was no correlation between severity of hepatitis or height of aminotransferase activities and the amount of HBsAg or HBcAg in hepatocytes but there was a positive correlation between amount of HBcAg and height of HBV-DNA and DNA polymerase activity in serum. Follow-up liver biopsies, taken 1 to 3 yr later, were available from 39 patients. HBcAg remained detectable in 25 of 26 patients with persistence of HBeAg but disappeared in 12 patients who had lost HBeAg. In nine patients, HBcAg was cytoplasmic as well as nuclear in distribution. Seven of these patients had an intense lobular hepatitis with marked elevations in aminotransferase activities. These findings indicate that the amount of HBcAg in liver correlates with the amount of serum hepatitis B virus as quantified by serum levels of DNA polymerase and HBV-DNA. The amount of nuclear HBcAg does not correlate with the severity of the liver disease, but the presence of cytoplasmic HBcAg usually reflects an active and severe ongoing hepatitis.
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PMID:Peroxidase-anti-peroxidase detection of hepatitis B surface and core antigen in liver biopsy specimens from patients with chronic type B hepatitis. 332 17

The subsets and expression of activation markers of inflammatory mononuclear cells in mild alcoholic liver disease were studied using monoclonal antibodies and an avidin-biotin-peroxidase complex (ABC) method. There were few B cells and monocytes in situ. Most of the mononuclear cells were of T cell origin, T4 and T8 positive cells being evenly distributed in a ratio of 2 to 1. This contrasts with the present and earlier findings on autoimmune liver diseases. The frequency of Ia (HLA-DR) positive cells varied between 15 and 30% of all mononuclear cells, which indicates activation of the local T cells. This implies that T cells in alcoholic fatty liver are not innocent bystanders but actively participate in the local inflammatory process. Staining for Tac, 4F2 and T9 was completely negative, however. These findings suggest that the local T cell activation may be incomplete and that it is not as extensive as in autoimmune liver diseases.
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PMID:Phenotypic in situ characterization of lymphocytes in mild alcoholic liver disease. 349 Jan 14


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