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)

Intravenous administration of soybean phosphatidylcholine liposomes containing different amounts of tocopherol acetate leads to a dose and time dependent increase of mouse liver tocopherol content, which was not observed when the preparation was given orally. When benzo[a]pyrene pretreated mice intoxicated with 400 mg/kg AAP were pretreated 2 h before with 1 g/kg phosphatidylcholine liposomes containing 4 mg/kg vitamin E acetate, these animals were protected against liver damage. Vitamin E alone or liposomes lacking vitamin E showed no protection. In an inflammatory liver disease model, i.e. fulminant hepatitis induced by intraperitoneal administration of 700 mg/kg galactosamine and 1 microgram/kg lipopolysaccharide phosphatidylcholine liposomes protected at a dose of 1 g/kg i.v. In this case, however, the protection was not due to the presence of vitamin E. These findings demonstrate the usefulness of phosphatidylcholine for liver protection and show that the protective spectrum is improved when they contain vitamin E. The data suggest that phosphatidylcholine is an excellent carrier for delivery of vitamin E to the liver.
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PMID:Hepatic uptake and antihepatotoxic properties of vitamin E and liposomes in the mouse. 236 59

Correcting action of vitamin E and it's short chain derivative on the activity of some mitochondria electron transport chain enzymes were investigated on models of acute and chronic toxic hepatitis. Inhibition of NADH- and succinate-cytochrome c oxidoreductase complexes activity was established in short term action of xenobiotics. Treatment of rats with CCl4 during 60 days lowered activity of NADH-cytochrome c oxidoreductase complex and significantly increased activity of succinate-cytochrome c oxidoreductase complex and succinate dehydrogenase. Obviously, as a result of long term influence of hepatotoxic agents switching over in rat mitochondria electron transport from NAD-dependent way of substrate oxidation to succinate-dependent way took place. This event could be a part of the body adaptation mechanisms. Vitamin E and its short chain analogue corrected activities of investigated enzymes of mitochondria liver in the animals with acute and chronic hepatitis.
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PMID:[Correction of the activity of certain enzymes in the rat liver mitochondrial electron transport chain by derivatives of alpha-tocopheryl acetate in toxic damage to the liver]. 1079 Oct 53

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

The immunocytograms of 166 patients with opiomania, primarily of the heroin variation, aged 15 to 19, were examined. 18 healthy teenagers of the same age were in the control group. The sampling comprised both patients without any signs of infectious diseases (86 persons) and patients with viral hepatitis B and C. The deviations of the immune-cellular status comprised, in drug addicts, a deficit of T-helpers and NK-cells as well as an increased quantity of "zero" lymphocytes. An essential reduction in the level of T-suppressors (killers) was additional found in the group of drug-addicts with viral hepatices. The signs of cytolysis of hepatocytes were detected in young heroin addicts. The contents of lipid peroxides was significantly higher in the blood plasma of teenagers abusing the opium drugs; while the concentration of antioxidant factor was as follows: Vitamin E, sulfhydric proteins and urate were found to be decreased. A reliable correlation was found between the changes of the quantity of T-helpers, T-suppresses (killers) and 0-lymphocytes, on the one hand, and the activity of hepatic transaminases, on the other hand, (for AST = 0.65-0.70; p < 0.01). The disorders in the immune-cellular status persist for as long as three to four weeks after the refusal from drug consumption; it is noteworthy, that their severity can essentially go up. The activity of 5'-nucleotidase, involved in the transformation of receptor signals in T- and B-lymphocytes, was histochemically studied in immunocytes. The activity of the enzyme essentially went down in both populations of lymphocytes by the 7th day of abstinence; it remained at the mentioned level up to the 14th day (in patients with hepatitis) or up to 21st day (in patients without hepatitis). Therefore, the quantitative deficit of immunocytes in drug addicts was accompanied, during the abstinence period, by an inhibition of their functional activity.
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PMID:[Disorders in the immune status and hepatic pathologies in young heroin addicts]. 1270 48