Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Role of lipid peroxidation on lysosomal instability in liver tissue was investiaged in an experimental model of D-galactosamine hepatitis in rats fed on vitamin E (V.E) deficient diet. Administration of D-galactisamine to V.E deficient rats resulted in a sudden increase of serum glutamic oxaloacetic transaminase (sGOT), glutamic pyruvic transaminase (sGPT), lipid peroxide value, as well as beta-glucuronidase and acid phosphatase activity examined as markers of lysosomal enzymes, when compared with control rats fed on V.E supplemented diet. Lipid peroxide in the liver tissue also showed significant increase in V.E deficient rats. In contrast, beta-glucuronidase and acid phosphatase in the liver tissue were found to decrease in V.E deficient rats by the administration of D-galactosamine, indicating that the enzymes in the lysosome were entirely released outside the liver cells as a result of cell destruction. It is concluded that the increase of lipid peroxide causes the instability of lysosomal membranes and releases various kinds of hydrolytic enzymes to lead further to cell damage. V.E might act on inhibiting lipid peroxidation to stabilize lysosomal membranes.
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PMID:Lipid peroxidation and lysosomal enzymes in D-galactosamine hepatitis and its protection by vitamin E. 44 84

beta-Glucuronidase, a lysosomal hydrolase, was purified from human liver tissue, and an enzyme-linked immunosorbent assay was developed using specific antibody against the enzyme. Using the assay procedure, the serum immunoreactive beta-glucuronidase (beta-glucuronidase) was determined in 190 patients with various liver diseases and in 53 healthy controls to examine whether or not the serum level of beta-glucuronidase would successfully reflect the degree of histological hepatic cell necrosis. beta-Glucuronidase was also determined at regular intervals in 28 patients with chronic hepatitis to investigate the clinical usefulness of serial measurement of the enzyme to predict the histological progression of hepatitis. These 28 patients could be subdivided into three groups, "continuously low type", "labile type" and "elevated type" according to the profiles of fluctuation of serum beta-glucuronidase values. Serum beta-glucuronidase was significantly increased in patients with hepatoma, liver cirrhosis and chronic active hepatitis compared with normal controls. There was significant positive correlation between the beta-glucuronidase and the degree of hepatic cell necrosis determined by histological observation, on the other hand, there was no statistical correlation between the transaminase activities and the degree of hepatic cell necrosis. It was confirmed in immunohistochemical study that the increased beta-glucuronidase in serum has been released from necrotic hepatic cells into blood stream. It was speculated that the elevation of serum transaminase activities had resulted from the alteration in the membrane permeability of hepatic cells rather than from hepatocellular necrosis. Histological progression of hepatitis was found in 8 of 10 patients (80%) of "labile" and "elevated type", while it was found only 3 of 18 patients (16.7%) of "continuously low type". These results suggested that the serial measurement of beta-glucuronidase could be used for an indicator to predict the histological progression of hepatitis.
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PMID:[Measurement of serum immunoreactive beta-glucuronidase: a possible serological marker for histological hepatic cell necrosis and to predict the histological progression of hepatitis]. 165 3

It is suggested that the important drugs rifampicin and halothane and the raised glucose levels in diabetes mellitus exert injurous effects on cells through a lysosomal mechanism. Further evidence is given of by time rifampicin induction of beta-glucuronidase and beta-N acetylglucosaminidase and its possible relation to hepatitis and pancreatitis. On the basis of preliminary data halothane may cause hepatitis connected to lysosomal enzyme release in the presence of other aggravating factors common to the perioperative period. The onset of diabetic vascular complications may be related to the similar raised levels of lysosomal enzymes found in insulin, drug and diet controlled disease. Release of these enzymes into plasma may be a marker of important changes in the lysosome, whether due to enzyme induction or damage, and could be a primary mechanism of many disease processes including some thought to be mainly autoimmune in character. Routine estimation in the clinical laboratory along with existing cytoplasmic and microsomally derived enzymes in the chemical screen would be a useful way of surveying lysosomal changes in the wide spectrum of disease in a general hospital.
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PMID:Rifampicin, halothane and glucose as mediators of lysosomal enzyme release and tissue damage. 341 3

Serum 3 beta-hydroxy-5-cholenoic acid (3 beta-OH-delta 5) was analyzed in 100 cases (90 patients with hepatobiliary diseases, 10 normal subjects) and its clinical significance investigated. The measurement of 3 beta-OH-delta 5 was performed by high performance liquid chromatography (HPLC) with immobilized 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) as the enzyme column. Esterified 3 beta-OH-delta 5 was measured after enzymatic hydrolysis with sulfatase and beta-glucuronidase. 3 beta-OH-delta 5 was hardly detected in normal cases. On the other hand, serum 3 beta-OH-delta 5 levels were remarkably high in cholestatic cases and also high in other cases with high bilirubin levels. The ratio of glycine- to taurine-conjugates (G/T ratio) was effective in discriminating cholestasis from hepatocellular damage such as in cases of acute hepatitis or fulminant hepatitis. More than 90% of the 3 beta-OH-delta 5, which is toxic, was sulfated or glucuronidated, suggesting detoxification by esterified bile acids. Significant increases of taurine-conjugated 3 beta-OH-delta 5 were observed in cases with pruritus, and a relationship between taurine-conjugated and pruritus was presumed. Therefore, analysis of 3 beta-OH-delta 5 is considered to be effective in clarifying the pathogenesis of hepatobiliary diseases.
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PMID:Clinical evaluation of serum 3 beta-hydroxy-5-cholenoic acid in hepatobiliary diseases. 347 20

In a survey the present possibilities are outlined to get knowledge about diseases of inner organs with the help of enzyme determinations in the urine. Here it is remarkable that changes of the enzyme excretion appear not only in renal disease with acute renal failure, pyelonephritis, glomerulonephritis, renal infarction and nephroptosis but are also to be observed in primarily extrarenal diseases such as diabetes mellitus, hyperthyroidism, thesaurismoses, myocardial infarction, hypertension, acute pancreatitis, epidemic hepatitis, liver cirrhosis, obstructive jaundice and rheumatoid arthritis. The causes of the changes of enzyme excretions are various. Since enzymes of different origin and localisation behave themselves variably, the simultaneous determination of a brush border marker (e.g. alanine aminopeptidase), a lysosomal enzyme (e.g. beta-glucuronidase or N-acetyl glucosaminidase) and a low molecular enzyme (e.g. lysozyme) is of use for the recognition of renal alterations. By the control of activities of urinary enzymes it is possible to get without risk informations about pathobiochemical processes in the kidney which are not to be gained by means of other methods.
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PMID:[Urinary enzyme excretion in diseases of the internal organs]. 636 87

Effects of single doses of kumari asav, kumari kalp, arogyavardhini and tamra bhasma on lysosomal enzymes (acid phosphatase and beta-glucuronidase) of rat liver and kidney were studied during hepatitis induced by single 0.3 ml/kg body wt dose of CCl4. Histologically all the drugs showed significant hepatoprotection. While acid phosphatase activities of liver and kidney were suppressed, activities of beta-glucuronidase were enhanced by these drugs. The results indicate that acid phosphatase and beta-glucuronidase behave differently, although they are lysosomal in nature.
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PMID:Effect of hepatoprotective ayurvedic drugs on lysosomal enzymes during hepatic injury induced by single dose of CCl4. 792 26

1-Naphthylisothiocyanate (ANIT) produces cholangiolitic hepatitis in rats. This injury is characterized by periportal bile duct and hepatic parenchymal cell necrosis with inflammatory cell involvement. In contrast, 2-naphthylisothiocyanate (BNIT) does not induce cholangiolitic hepatitis. The mechanism(s) involved in ANIT-induced hepatic injury remain to be elucidated. To investigate this difference in toxicity further, we examined the cytotoxicity of ANIT and BNIT in primary rat hepatocyte cultures. Since neutrophils (PMNs) are required for the development of ANIT-induced cholangiolitic hepatitis in vivo, we also examined the potential for PMNs to modulate ANIT and BNIT cytotoxicity in rat hepatocyte-PMN cocultures. Both ANIT and BNIT injured rat hepatocytes within the range of concentrations examined (0-100 microM); however, BNIT was more potent. The presence of PMNs did not significantly influence the hepatocellular injury produced by either naphthylisothiocyanate (NIT). In an attempt to clarify the disparity between these results in vitro and observations reported in vivo, we examined, in hepatocyte PMN cocultures, the cytotoxic potential of bile collected from NIT-treated rats. Bile from BNIT-treated rats was markedly more cytotoxic to hepatocytes than was bile from ANIT-treated rats. As was observed in earlier experiments, the inclusion of PMNs had no effect on the hepatocellular toxicity of bile from NIT-treated rats. These findings prompted evaluation of the effect of NITs on rat PMNs. ANIT (1 and 10 microM) had no effect on phorbal myristate acetate (PMA)-induced superoxide production by PMNs, whereas BNIT (1 and 10 microM) markedly inhibited PMA-induced superoxide production. In contrast, ANIT and BNIT were equally effective at inhibiting f-met-leu-phe (fMLP)-induced PMN degranulation (beta-glucuronidase release). Altogether, the relative NIT toxicity observed in hepatocyte primary cultures is contrary to reports of hepatotoxic potential of these NITs in vivo. The PMN-dependence of ANIT hepatotoxicity in vivo was not reproduced in hepatocyte-PMN cocultures exposed to ANIT, suggesting that the PMN dependence in vivo involves factors not present in hepatocyte PMN cocultures. The greater PMN inhibitory effect of BNIT may, in part, underlie its inability to elicit the PMN-dependent liver injury in vivo that characterizes ANIT-induced cholangiolitic hepatitis.
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PMID:Cytotoxicity of naphthylisothiocyanates in rat hepatocyte-neutrophil cocultures. 970 17

Free-radical-mediated oxidant damage can contribute to acute hepatitis. Vitamin E, a classic antioxidant, has been tested as a therapy for rodent acute hepatitis, but the protection achieved has not been complete. This study demonstrated that in rats, sodium diethyldithiocarbamate (DDC), a potent antioxidant, strongly depressed galactosamine-induced hepatitis in terms of serum alanine amino transferase activities and bile acids, though not in terms of serum beta-glucuronidase activities. A potential limitation for DDC use in humans, inhibition of copper metalloenzyme activities, did occur at the DDC dose used here. However, these effects were not severe. Thus, DDC could make a useful short term therapeutic drug for acute hepatitis.
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PMID:Diethyldithiocarbamate inhibition of galactosamine-induced hepatitis in rats. 1188 24

Activities of the enzymes beta-glucuronidase, acid phosphatase, acid DNAase, acid RNAase, and acid protease have been measured in the lysosomal and supernatant fractions of mouse liver cells and monkey kidney cells before and after infection with mouse hepatitis virus and vaccinia virus, respectively. In the infected cells there was easily measurable release of lysosomal enzymes into the supernatant fraction. Evidence was presented that this is not an artefact of homogenization and precedes cell degeneration demonstrable histologically. It is suggested that release of lysosomal enzymes may explain some of the biochemical changes found in infected cells and may contribute to the cytopathic effects of some viruses.
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PMID:Activation of lysosomal enzymes in virus-infected cells and its possible relationship to cytopathic effects. 1401 75