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 authors studied the assimilation of nitrogen preparations--moriamin S-2 and "improved" caseine hydrolysate in parenternal administration to 100 albino rats. Healthy animals and those with toxic affection of the liver induced with CCl4 were experimented upon. In healthy animals administration of nitrogen preparations led to the change of negative nitrogen balance into a positive one, normalized the content of blood and tissue amine nitrogen deranged in protein deficiency. Assimilation of nitrogen preparations fell considerably in toxic hepatitis. An 8-day parenteral nutrition failed to change the negative nitrogen balance into positive, and did not eliminate hypoproteinemia; however, it normalized the amine nitrogen concentration in the blood and tissues.
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PMID:[Anabolic effectiveness of nitrogenous preparations for parenteral nutrition in the presence of toxic liver damage]. 9 94

Enzyme deviations in injured livers were studied by analyzing isozyme patterns of phosphorylase using a newly developed electrophoretic method, which separates six molecular species of this enzyme, i.e. M,FM,F,L,L', and FL'. In hepatic injuries caused by CCl4 and galactosamine intoxications of rats, F appeared in early stages and L' (and FL') in later stages of the injuries with a concurrent decrease or loss of L, which is a sole isozyme component of adult liver. In injured livers of patients with hepatitis and cirrhosis of the liver, increases in FL' activity were also found. Appearance of F was found only in hepatocellular carcinoma. The results obtained with phosphorylase isozyme analysis support the idea that an undifferentiated gene expression takes place in the injured livers of non-malignant hepatic disorders.
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PMID:Studies of liver phosphorylase in hepatic injuries II. Alteration in isozyme pattern. 15 93

Drugs and other chemicals are usually metabolized in the liver in the drug-metabolizing enzyme system. The metabolites sometimes bind with cellular macromolecules and injure the cell directly or serve as new antigens to create immunologic injury in a delayed fashion. The immediate or toxic injury is dose-dependent, predictable and zonal in the liver lobule, usually in the central region. Carbon tetrachloride intoxication and acetaminophen overdose are examples of injury resulting from microsomal metabolism. Other injuries related to microsomal metabolism are those produced by vinyl chloride in polymerization plant workers and by methotrexate in psoriatics or leukemic children. Most adverse drug reactions affecting the liver and producing jaundice are unpredictable, delayed in onset, and only hypothetically related to microsomal metabolism in some instances. The two main types are cholestasis and viral-hepatitis-like. The former may be in a pure form, in which case it may be partly dose-dependent, or in a form mixed with hepatitis. Many drugs produce cholestasis in a small percentage of persons, and because the reaction is benign, albeit prolonged at times, such drugs continue to be used. The viral-hepatitis-like reaction involves few drugs and affects few persons, but can be fatal. The recognition that chronic hepatitis can be caused by drugs such as oxyphenisatin, alpha-methyldopa, and isoniazid has added a new dimension to the clinical problem of adverse drug reactions, which may extend to widely used and commonly available agents like aspirin.
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PMID:Hepatic drug metabolism and adverse hepatic drug reactions. 17 22

Liver protocallagen proline hydroxylase activity (PPH activity) was determined in patients with various liver diseases, CCl4-induced liver fibrosis rats and cholin deficiency (tcd) fatty liver rats. The following results were obtained: Liver PPH activity in patients with chronic hepatitis was higher than that in patients with acute hepatitis, while the activity in patients with liver cirrhosis was much higher than that in patients with chronic hepatitis. The activity was higher in patients with chronic active hepatitis than in those with chronic inactive hepatitis. Patients with active and progressive liver cirrhosis were found to have an especially high PPH activity, in whom the activity reflected well the degree of liver fibrosis. Even though fibrosis in persistent hepatitis was almost negligible or slight, the degree of liver PPH activity in persistent hepatitis was similar to that in liver cirrhosis. Liver PPH activities in CCl4-induced liver fibrosis rats and CD fatty liver rats elevated proportionally to the lapse of time. Whilst liver PPH activity in rats of CD fatty liver without fibrosis in 23 to 31 weeks after the start of the experiment was slightly lower than that in rats of CD fatty liver with fibrosis. But liver PPH activity of the former was considerably higher than that of control rats.
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PMID:Liver protocollagen proline hydroxylase in human liver diseases and experimental liver fibrosis. 19 57

Parameters of oxidative phosphorylation, the rate of respiration in various metabolic conditions as well as an activity and stability of mitochondrial polyenzyme systems were altered in rats with experimental hepatitis, treated with CCl4. Proteins and phospholipids from mitochondrial membranes proved to be more susceptible to the effect of trypsin and phospholipase D. Kinetics of cytochrome C desorption from membranes and mitochondria demonstrated that capacity of these membranes to confine the exogenous proteins was altered in hepatitis.
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PMID:[Functioning of rat liver mitochondria in hepatitis]. 21 41

The effect of lysosomotropic agent--sodium aurothiomalate on liver damage and lysosomal changes during acute toxic hepatitis was studied. Combined administration of sodium aurothiomalete led to less extensive necrosis and to widening dystrophic areas in the hepatic parenchyma. Solubilization of the acid RNA-ase activity was decreased, and nonsedimentable activities of beta-galactosidase, cathepsin D were the same as in acute CCl4-hepatitis.
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PMID:[Effect of sodium aurothiomalate in acute toxic hepatitis]. 40 45

The nitrogen metabolism in rats with toxic affection of the liver caused by administration of CCl4 was studied as affected by the amino acid mixture moriamine S-2. It is established that with toxic hepatitis the nitrogen metabolism is sharply disturbed, especially during protein deficiency. The following evidences for this fact: a rise in the depth of the nitrogen negative balance, an increase in the intensity of amine nitrogen and ammonia excretion with urea as well as an increase in the amount of amine nitrogen in blood and tissues with a simultaneous decrease in the content of protein. The parenteral administration of the amino acid mixture for eight days to the animals with a toxic affection of the liver is more effective when nitrogen preparation is combined with the group B vitamin, vitamin C, insulin, nerobolyl and sirepar.
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PMID:[Correction of nitrogen metabolism in rats with toxic hepatitis by parenteral administration of an amino acid mixture]. 42 34

Physical and chemical properties of the rat liver lysosomes with single Triton WR 1339 overloading were studied during the administration of a detergent to intact rats and those with acute toxic hepatitis. Administration of the latter to intact animals was accompanied by a reduction of the floating density of the particles, solubilization of the lysosome enzymes and by increased fragility of the particles in the hypotonic medium. Lysosomes of the hepatocytes in rats with toxic hepatitis also displayed signs of overloading of the vacuolar apparatus with the preparation administered. The most pronounced solubilization of the lysosomal enzymes beta-galactosidase, acid RNA-ase, cathepsin D--was noted in case of combined action of CCl4 and Triton WR 1339 24, 48, 72 hours and 7 days after the CCl4 poisoning. Possible consequences of overloading of the vacuolar apparatus of the rat hepatocytes are discussed.
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PMID:[Role of vacuolar apparatus overload in lysosomal changes in liver cells in acute toxic hepatitis]. 42 73

The effect of cytidine and uridine on the reparative processes in the rat liver in experimental hepatitis induced by CCl was studied. Combined administration of uridine or cytidine with CCl4 during 7 days does not prevent the liver affection. The subsequent nucleoside treatment (up to 15 and 20 days) accelerates to a different degree the reparative processes after CCl4 withdrawal. Thus, cytidine provokes marked hypertrophy of regenerated hepatocytes accompanied by proliferation of the mesenchymal elements, not followed, however, by recovery of the conjugative and excretory liver functions. Uridine, in contrast to cytidine, promotes more rapid normalization of these functions though the organ structure regeneration is not complete.
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PMID:[Effect of cytidine and uridine on liver regeneration in rats poisoned by carbon tetrachloride]. 51 7

A preliminary injection of triton WR 1339 protectively influenced the chronic toxic CCl4-hepatitis. The ultrastructural peculiarities were close to the normal ones in hepatocytes, in addition to the increased triglyceride rejection from cells by means of autophagy. The revealed stimulation signs of pinocytosis in hepatocytes and the Kupfer cells are accompanied by the activation of the Golgi complex and, probably, by the increased protein catabolism in lysosomes. The signs of phagocytosis increase in the Kupfer cells were determined. It is supposed that the marked ultrastructural peculiarities of liver cells reflect a more effective restoration or a lesser injury under the influence of triton WR 1339.
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PMID:[Effect of triton WR 1339 on the ultrastructure of liver parenchymal and stromal cells in rats with chronic toxic hepatitis]. 60 65


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