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)

Distinguishing between obstructive (surgical) and hepatocellular (medical) jaundice is sometimes impossible using the relatively simple diagnostic means of history, physical examination and liver function tests. In an attempt to reduce the number of jaundiced patients in need of complex and expensive diagnostic procedures, we investigated the use of the plasma amino acid pattern in the diagnosis of jaundice. Jaundiced rats with galactosamine-induced hepatitis and seven patients with acute onset hepatitis presented a plasma amino acid pattern in which most all amino acid levels were elevated except for arginine in the rat and branched chain amino acids in the patients. Rats jaundiced due to common bile duct ligation and seven patients with obstructive jaundice proved at surgery exhibited a near-normal amino acid pattern. These experimental and clinical data demonstrate very clear qualitative and quantitative differences in plasma amino acid patterns of hepatocellular and obstructive jaundice, with the latter exhibiting an almost-normal pattern. We suggest the use of the plasma amino acid pattern as a useful adjunct in the differential diagnosis of medical and surgical jaundice.
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PMID:Plasma amino acid analysis in the differential diagnosis of jaundice. 735 Aug 38

1. D-Galactosamine-HCl induces toxic hepatitis in the rat and was used as a model to study some aspects of iron metabolism during liver cell damage. Some changes in iron metabolism were similar to those encountered in human acute viral hepatitis. 2. During the first 3 days of liver cell damage induced by galactosamine, liver depot iron and especially ferritin iron decreased by approximately 20%. Plasma ferritin rose, with a peak mean value which was approximately 20 times the concentration measured in normal rats. 3. During the acute phase, plasma ferritin did not accurately reflect the change in the level of liver depot iron. 4. During and after the acute phase, liver depot iron increased after an initial decrease. The non-ferritin depot iron fraction was elevated approximately 75% compared with the value in normal rats. This increase in non-ferritin iron was probably caused by increased erythrocyte catabolism in the liver and recapture followed by catabolism of liver ferritin that had leaked into the blood.
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PMID:Rat liver storage iron and plasma ferritin during D-galactosamine-HCl-induced hepatitis. 737 57

1. The anti-inflammatory and hepatoprotective efficacy of CuPu(Py)2 ((N,N'-bis(2-pyridyl-methylene)-1,4-butanediamine) (N,N',N",N")-Cu2+), a serum-stable, copper-di-Schiffbase active centre analogue of Cu2Zn2 superoxide dismutase was tested in male NMNR mice suffering from endotoxin/galactosamine-induced hepatitis. 2. Parameters including the activities of serum transaminases and sorbitol-dehydrogenase as well as the levels of reactive oxygen and nitrogen intermediates which were used to quantify the disease activity. 3. A dose-dependent inhibition of hepatic enzyme release was noted in the presence of 0.1-10 mg/kg of CuPu(Py)2. 4. The release of transaminases from damaged liver cells was reduced by 68% and paralleled the reduction of serum levels of nitric oxides. 5. Elevated levels of reactive oxygen species were normalized to those healthy controls. 6. The copper-free apochelate Pu(Py)2, which is unable to dismutate superoxide, did not display any anti-inflammatory reactivity.
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PMID:Hepatoprotective reactivity of a copper-di-Schiffbase active centre analogue of Cu2Zn2 superoxide dismutase. 759 Jan 16

The relationship between the plasma concentration and the anti-inflammatory effect of naproxen (CAS 22204-53-1) after oral administration of a 6 mg.kg-1 dose was studied in rats with galactosamine-induced acute hepatitis and under control conditions. In control animals naproxen peak plasma levels of 35 +/- 0.4 micrograms.ml-1 were reached in 0.5 +/- 0 h. Concentration then decayed, half-life being 5.2 +/- 0.4 h. AUC was 131 +/- 5 micrograms.h.ml-1. In intoxicated rats peak plasma levels of 29 +/- 0.3 micrograms.ml-1 were reached in 0.7 +/- 0.1 h, half-life was increased to 11.1 +/- 1.3 h, and the AUC reached 259 +/- 21 micrograms.h.ml-1. In control rats the protective effect of naproxen against carrageenan-induced inflammation increased slowly, reaching a maximum of 38% in 4 h. The protective effect against plasma concentration curve exhibited a clear counterclockwise hysteresis, probably due to a slow naproxen transport from the circulation to its site of action. In animals with hepatitis, the protective effect remained quite constant at about 40% despite variations in plasma levels, probably because the maximal effect was reached. No clear hysteresis was observed in the effect-plasma concentration curve, suggesting that naproxen arrival to its site of action was faster. Results show that the relationship between naproxen plasma concentration and its anti-inflammatory effect is complex and therefore predictions on the pharmacological response in liver damage cannot be readily made by solely considering pharmacokinetic data.
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PMID:Relationship between naproxen plasma concentration and its anti-inflammatory effect in experimental hepatitis. 761 58

Manganese (II) N,N'-dipyridoxylethylenediamine-N,N'-diacetate 5,5'-bis(phosphate) (DPDP) is a paramagnetic magnetic resonance (MR) contrast agent that enhances the liver and is predominantly excreted through the biliary tree. The authors evaluated its utility in diffuse liver disease by assessing liver and gallbladder enhancement in 24 rabbits. Total (n = 6) or segmental (n = 6) biliary occlusion or galactosamine-induced hepatitis (n = 6) was induced 3 days before imaging. Six rabbits served as normal controls. T1- and T2-weighted axial MR images were acquired at baseline, followed by T1-weighted images every 10 minutes for 1 hour after the intravenous administration of 20 mumol/kg Mn-DPDP. Except for the segmental occlusion group, the baseline study did not allow distinction between normal and abnormal livers. The temporal hepatic enhancement pattern was statistically different for each group. The normal, segmental occlusion, and hepatitis groups showed patterns similar to one another but markedly higher signal intensity than the total-occlusion group throughout the observation period. In contrast, the gallbladder showed a greater difference in both degree of enhancement and time to peak enhancement among the four groups. Mn-DPDP produces a temporal hepatic enhancement pattern that allows recognition of markedly impaired livers, and gallbladder enhancement patterns that allow distinction of more subtly impaired livers.
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PMID:MR imaging assessment of experimental hepatic dysfunction with Mn-DPDP. 769

The survival rate for acute hepatic failure induced by Propionibacterium acnes and lipopolysaccharide (LPS) was increased when a hot water extract from the flowers of Inula britannica L. subsp. japonica Kitam. was injected into the experimental hepatitis mice, and anti-hepatitis substances could be extracted with CHCl3. The CHCl3 extract from I.britannica was fractionated and anti-hepatitis fractions IB-3-2 and IB-3-3 were obtained. IB-3-3 had the most potent anti-hepatitis activity among the fractions but further purification of the active compound was not achieved because of the low yield. IB-3-2 contained only one substance which was identified to be taraxasteryl acetate by 1H- and 13C-NMR and MS. Taraxasteryl acetate showed potent preventive activity against acute hepatic failure induced by P.acnes and LPS in a dose-dependent manner, however deacetylation and modification of the olefinic bonds significantly decreased the anti-hepatitis activity of taraxasteryl acetate. Taraxasteryl acetate also inhibited the increment of plasma transaminase on acute hepatic failure induced by carbon tetrachloride (CCl4) or D-galactosamine. From a histological study it appeared that degeneration and necrosis, which were observed in the liver from CCl4 mice, were not found in the liver cells from taraxasteryl acetate treated mice. These results indicates that taraxasteryl acetate shows preventive effects on experimental hepatitis caused by either immunologically induced injuries or hepatotoxic chemicals.
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PMID:Preventive effect of taraxasteryl acetate from Inula britannica subsp. japonica on experimental hepatitis in vivo. 1725 90

Galactosamine-induced hepatitis caused a marked increase in plasma lactate and pyruvate, but completely abolished the increase in ketone bodies in the rat exposed to an 8000 m simulated altitude. Plasma free fatty acid as the precursor of ketone bodies was higher in the galactosamine-treated rats during and after an exposure to 8000 m altitude. Treatment of the rat with galactosamine markedly reduced activities of citrate synthase, fumarase, glutamate dehydrogenase and fructose 1,6-bisphosphatase, but increased hexokinase and glucose 6-phosphate dehydrogenase in the liver. The effect of galactosamine-induced hepatitis on the energy metabolism can be explained by a reduction of mitochondrial oxidative enzymes and gluconeogenesis, and involves a shift of the aerobic metabolism to anaerobic glycolysis at high altitude.
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PMID:Effect of galactosamine-induced hepatitis on the aerobic and anaerobic metabolism of the rat exposed to high-altitude hypoxia. 774 7

The hepatoprotective effects of Ixeris chinensis (Thunb.) Nak. were studied on acute hepatitis induced in mice by a single dose of carbon tetrachloride (31.25 microliters/kg, ip) or acetaminophen (600 mg/kg, ip), and in rats by a single dose of beta-D-galactosamine (188 mg/kg, ip). Hepatoprotective activity was monitored by estimating the serum transaminases (SGOT and SGPT) levels and histopathological changes in the livers of experimental animals. The Ixeris chinensis (Thunb.) Nak. extracts significantly inhibited the acute elevation of serum transaminases. Histopathologically, the crude I. chinensis extract significantly ameliorated hepatotoxin-induced histopathological changes in the livers of experimental animals. All pharmacological and histopathological effects of Ixeris chinensis (Thunb.) Nak. were compared with Bupleurum chinense DC., which has been previously reported as a treatment herb for hepatitis.
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PMID:Hepatoprotective effects of Taiwan folk medicine: Ixeris chinensis (Thunb.) Nak. on experimental liver injuries. 787 36

Zn deficiency is hypothesized to produce poor resistance to injury involving oxidative stress. This could occur by impairing Zn antioxidant function(s) or by indirectly limiting adaptive protective mechanisms such as a rise in acute-phase proteins. The present study examined rats fed diets adequate or moderately low in Zn (4 or 25 micrograms/g diet) for 9 d. The lower intake produced a mild Zn deficiency based on body weight, plasma Zn and plasma alkaline phosphatase (EC 3.1.3.1) activity. Galactosamine injection, an oxidative stress, produced much more liver injury in the mildly Zn-deficient rats. However, injury was strongly inhibited in rats from each dietary group by an acute-phase response due to turpentine-induced leg inflammation. Mild Zn deficiency did not prevent a rise in levels of the acute-phase protein caeruloplasmin (EC 1.16.3.1), but did limit the usual inflammation-induced rise in hepatic levels of metallothionein, a Zn protein with possible antioxidant function. In conclusion, high degrees of galactosamine-induced hepatitis were associated with mild Zn deficiency, but the liver injury was blocked by prior stimulation of an acute-phase response, regardless of Zn status.
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PMID:Effects of mild zinc deficiency, plus or minus an acute-phase response, on galactosamine-induced hepatitis in rats. 798 91

The changes in the concentrations of reduced (GSH) and oxidized glutathione (GSSG) in the plasma as well as in the liver were investigated in rats with endotoxin hepatitis. Hepatitis was induced by intraperitoneal co-administration of small doses of Escherichia coli endotoxin and D-galactosamine. In the liver, the concentration of GSH decreased and that of GSSG increased 12 hr later. In the plasma taken from the right atrium, the concentration of both GSH and GSSG increased. The GSH/GSSG ratio in the plasma decreased, as it did in the liver. The net sinusoidal efflux of GSH and GSSG from the liver was calculated by subtracting their concentrations in plasma of the infrahepatic, suprarenal inferior vena cava from those of the suprahepatic inferior vena cava. The efflux started to increase as early as 2-4 hr after the injection of the toxins. In contrast, a leakage of alanine aminotransferase, an elongation of prothrombin time, an inhibition of starvation ketosis, and an increase in serum concentration of total bilirubin were detected as late as 6-8 hr after the injection. We conclude that endotoxin/D-galactosamine hepatitis induced an increase in plasma concentrations of GSH as well as GSSG by increasing the efflux of these peptides from the liver, and that changes in plasma glutathione status might be useful and sensitive markers for liver damage.
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PMID:Increased sinusoidal efflux of reduced and oxidized glutathione in rats with endotoxin/D-galactosamine hepatitis. 802 75


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