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)

The liver microsomal delta 9 and delta 6 desaturase activities have been studied in rats with carbon tetrachloride-induced hepatitis. Immediately after poisoning, significant decreases were observed for both types of desaturase activity. However, recovery kinetics were slower for the delta 6 desaturase than for the delta 9 desaturase. The activities of NADH-ferricyanide and NADH-cytochrome C reductases, proteins involved in the electron transfers associated with microsomal desaturation, were also measured. There was a fall in both activities after poisoning, but this decrease was less than that of the desaturase activities.
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PMID:Hepatic delta 9 and delta 6 desaturase activities during the recovery period following carbon tetrachloride poisoning. 610 78

Alcohol is the most significant liver poison. Its degradation takes above all place by the alcohol dehydrogenase and the microsomal alcohol-oxidizing system. In the first step of degradation acetaldehyde develops which in enrichment evokes immediately toxic defects on the mitochondrias of the cells of the liver parenchyma and thus introduces a vicious circle. Furthermore, an increased affection of pharmacometabolites as a sequel of the alcohol-conditioned enzyme induction may lead to a defect. Alcohol influences intermediary metabolic functions: the gluconeogenesis is inhibited, multi-layer disturbances in the lipid metabolism lead to fatty degeneration of the liver. A hyperuricaemia results from overproduction in the liver as well as from decreased renal excretion. The proline formation is increased. Distinct increase of the gamma-GT-activity is an early and relatively specific indicator of the alcoholic liver defect. Morphologic and clinical manifestations are fatty degeneration of the liver, hepatitis based on fatty degeneration of the liver and cirrhosis. Apart from dose and duration of the alcohol intake additional factors require consideration. The author adopts a definite attitude to etiopathogeneis and therapeutic possibilities.
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PMID:[Alcohol and the liver]. 611 57

The purified Schistosoma mansoni adult microsomal antigen, MAMA, was used in the quantitative single-tube kinetic dependent enzyme-linked immunosorbent assay (k-ELISA) to measure antibody levels of various human patient sera. The 511 serum specimens tested were from patients with both homologous and heterologous infections. Sera from U.S., Egyptian, Brazilian, and Puerto Rican patients infected with S. mansoni reacted strongly with MAMA. Chinese patients infected with S. japonicum, and Nigerians or Egyptians infected with S. haematobium produced much lower responses to this antigen than those infected with S. mansoni. Sera from patients with echinococcosis, filariasis, paragonimiasis, clonorchiasis, trichinosis, amebiasis, and hepatitis and from healthy uninfected control individuals generally contained no detectable antibodies against this antigen. The S. mansoni adult microsomal antigen, MAMA, therefore, appears to be a highly potent and specific reagent for the serodiagnosis of S. mansoni infections.
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PMID:Schistosoma mansoni adult microsomal antigens, a serologic reagent. II. Specificity of antibody responses to the S. mansoni microsomal antigen (MAMA). 618 78

The sera of 131 patients with anti-liver-kidney microsome antibodies (anti-LKM) detected between 1973 and 1979 in two different laboratories were re-examined. (1) Eighty-six anti-LKM corresponded to the description given by Rizzetto, Swana & Doniach (1973), with a pattern of fluorescence predominating on the 3rd portion of the proximal tubules (P3). This group comprised 45 cases of idiopathic chronic hepatitis or idiopathic cirrhosis and one case of halothane-induced hepatitis. (2) Forty-five anti-LKM gave a different pattern on male mouse liver and male rat kidney: (a) fluorescence was greater on centrolobular than on periportal hepatocytes; (b) the first and second portions of proximal tubules (P1 and P2) predominated over P3; (c) P1 fluorescence was equally intense as P2 and (d) P3 cells were heterogeneous with one cell out of 20 more positive than the rest. Absorption tests confirmed that the corresponding antigen was also present in the liver microsomal fraction. A retrospective clinical study discovered tienilic acid-induced hepatitis in all cases. We suggest naming this new antibody 'anti-LKM2'.
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PMID:A new anti-liver-kidney microsome antibody (anti-LKM2) in tienilic acid-induced hepatitis. 636 59

Various autoantibodies against different components of the hepatocytes have been demonstrated in chronic active hepatitis (CAH) which is an etiologically heterogeneous disease. These antibodies are essentially antinuclear antibodies (ANA), antibodies against liver cell membranes (LMA), antibodies against a microsomal antigen from liver and kidney (LKM), antibodies against soluble liver antigen (SLA) and antimitochondrial antibodies (AMA). These various autoantibodies mentioned could not be demonstrated in 18 patients with clearly established acute and 27 patients with clearly established acute and 27 patients with clearly established chronic hepatitis non-A-non-B. In addition these autoantibodies could not be found in our own cases of clearly established hepatitis non-A-non-B after the acute stage of the disease. Testing for the presence of these antibodies thus helps essentially to differentiate the autoimmunologically caused form of CAH from the CAH non-A-non-B.
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PMID:[Significance of autoantibodies in the diagnosis of non-A, non-B hepatitis]. 643 3

Microsomal antigens and corresponding antibodies are predominantly detected following halothane hepatitis and chronic active hepatitis with autoimmune markers. In the case of acute hepatitis B reported by us, complexed microsomal antigens were found during active disease, gradually clearing with seroconversion of microsomal markers and improvement of liver function.
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PMID:[Complexed microsomal antigens in acute hepatitis B (author's transl)]. 645 21

This study evaluated the subchronic (14-day) toxicity of selected (0.2, 1.0, and 4.0 mg/kg) daily subcutaneous injections of diethylstilbestrol (DES) in female (C57B1/6 X C3H)F1 mice. Parameters observed included body and organ weights, gross organ morphology, histopathology, clinical chemistry, and hepatic microsomal enzyme activities. The liver, bone marrow, and thymus are major target organs for DES. Liver enlargement, with associated histopathological changes consistent with mild hepatitis, centrolobular necrosis, and sinusoidal changes were observed. Supporting the histological changes were alterations in serum enzyme levels and microsomal enzyme activity. Bone marrow changes included decreases in the number of cells as well as the number of colony forming units per gram stem cells. Toxicity to the thymus was evidenced by decreased thymic weights and lymphocyte depletion. The hepatic and thymic effects were observed at the lowest (0.2 mg/kg) dose. Although all parameters were not assessed for recovery, those that were evaluated returned to control levels by thirty days after treatment.
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PMID:Subchronic toxicology of diethystilbestrol in the mouse. 662 66

Three consecutive head nurses developed liver injury after years of handling cytostatic drugs. They had neurological symptoms associated with elevated serum alanine amino-transferase (ALAT) and alkaline phosphatase (ALP) levels. Liver histology showed portal hepatitis with piecemeal necrosis in one of them, the others had hepatic fibrosis and fat accumulation. The subjects' livers were metabolically active as reflected by adaptive and toxic changes in cellular ultrastructure. After withdrawal of the drugs, serum ALAT and ALP values fluctuated between normal and 2-3 times elevated. Follow-up biopsies demonstrated an increase in collagen fibres and a decrease in microsomal enzyme activity, as reflected by arylhydrocarbon hydroxylase activity in vitro. The findings suggest that handling of cytostatic drugs may insidiously damage the liver, which, with time, seems to lead to irreversible fibrosis.
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PMID:Liver damage in nurses handling cytostatic agents. 666 24

The function of microsomal destructing medicaments enzyme systems of the liver cell under hormonal contraception was objectified with the help of the aminopyrine test. After the oral administration of 9 mg dimethylaminoantipyrine (DMAAP) per kg body-weight together with 111 kBq 14C-DMAAP the elimination of 14CO2 was measured on the basis of the decrease of the radioactivity in the expiration air (respiration test). The plasma levels of DMAAP and its metabolites were measured, too. The two measurements lasted 5 hours. In contrast to a control group consisting of 8 women with healthy liver who were not ovulostatically treated (half-value time 14CO2-DMAAP 2.9 +/- 0.8 h, plasma 2.2 +/- 0.5 h) in 20 test women with healthy liver under ovulation inhibitors the elimination of 14CO2-DMAAP with 4.7 +/- 1.6 was clearly (alpha less than 0.01), the plasma elimination with 3.0 +/- 0.8 h was slightly retarded (alpha less than 0.05). In 19 patients with histologically ascertained chronic hepatopathies of above all insignificant degree of severity (13 degenerative lesions of liver parenchyma, 3 fatty livers stage I or II, 1 chronic active hepatitis each, chronic persisting hepatitis and cirrhosis) under hormonal contraception a half-value time of the 14CO2 elimination (alpha less than 0.001) prolonged to 5.0 +/- 1.5 h and a prolongation of the plasma elimination to 3.8 +/- (alpha less than 0.05). In 9 women in double examinations the 14CO2 elimination of the DMAAP after discontinuation of the application of ovulation inhibitors was compared with the values obtained under hormonal contraception and a regression of the retarded excretion in the expiration air (4.2 +/- 2.3 less than 5.1 +/- 1.2 h) and plasma (2.6 +/- 0.7 less than 3.4 +/- 1.7) was proved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hepatic clearance of aminopyrine in the evaluation of liver function in hormonal contraception]. 667 Mar 37

The authors have studied the action of fluorine, administered by inhalation, on the liver metabolism of a chemical carcinogen: dimethylnitrosamine (DMN). The results demonstrate a decrease in the level of cytochrome P450 and in the activity of benzo(a)pyrene hydroxylase in animals treated with DMN or DMN + HF. The greater inhibition in the presence of HF is paralleled by a decrease in the weight of the liver and in the synthesis of liver microsomal proteins. This reduction of activity (with the exception of dimethylnitrosamine demethylase which is unaffected) is supported by the result of the histological examinations showing two different types of lesion-necrotic toxic hepatitis and post-hepatitic cirrhosis - the frequency of which is much higher in the presence of fluorine.
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PMID:[Effect of HF on the hepatic metabolism of dimethylnitrosamine in the rat]. 667 13


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