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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Galactosamine, a selective hepatotoxin, produces in rats histologic alterations, which show the characteristics of severe human viral hepatitis. In the present study the efficacy of two different cofactor regimens (coenzyme A, NAD, alpha lipoic-acid, cocarboxylase) in rats with fulminant galactosamine hepatitis were tested. The results showed an improvement of the short-term survival with a short-term treatment and definitely better survival with a long-term regimen with cofactors.
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PMID:Effect of coenzyme-A, NAD, alpha lipoic-acid and cocarboxylase on survival of rats with galactosamine-induced severe hepatitis. 392 31

We have previously shown that supplemental vitamin E has a cytoprotective effect in the liver of rats with chronic CCL4-induced liver cirrhosis. In this study, we hypothesized that vitamin E would have a protective effect in acute liver injury induced by D-galactosamine. D-Galactosamine-induced injury has been thought to be due to a synergistic direct toxic effect and presence of intestinal bacteria and/or endotoxins. D-Galactosamine was used to induce acute "hepatitis" (1.5-2.0 g/Kg body weight, ip). Rats were placed on either standard chow or the same chow supplemented with vitamin E (300 mg DL-alpha-tocopherol/Kg diet) and 6 days later were given D-galactosamine. There was significantly improved early (5-day) survival and late (14-day) survival in the vitamin E-supplemented group. The vitamin E beneficial effect was manifested also by decreased liver fat and collagen content and decreased SGPT level. Because bacterial endotoxins have been implicated as playing a role in the pathogenesis of D-galactosamine hepatitis, the same experiment was carried out using germ-free and conventional rats. There was significantly improved survival in both the germ-free and conventional vitamin E-supplemented groups both at 5 and 14 days. There was no significant difference between conventional and germ-free rats with or without vitamin E supplementation. In summary (a) vitamin E improves the early fat and collagen accumulation in the liver, decreases SGPT level, and improves survival in the D-galactosamine experimental model of acute liver injury in both conventional and germ-free rats; and (b) D-galactosamine toxicity is probably not mediated through intestinal bacteria and/or endotoxins.
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PMID:Protective effect of vitamin E in rats with acute liver injury. 395 25

1. In confirmation of previous work, administration of d(+)-galactosamine (0.5-0.75g/kg body wt.) to rats caused a hepatitis with histological evidence of liver damage and a 9-fold rise in aspartate aminotransferase activity in serum. 2. There was a significant elevation of blood lactate and pyruvate concentrations in 24h-starved rats treated with galactosamine but no change in the [lactate]/[pyruvate] ratio. 3-Hydroxybutyrate and acetoacetate concentrations in blood were decreased. 3. The changes in the concentrations of lactate, pyruvate and ketone bodies in the freeze-clamped liver were parallel to those observed in the blood. 4. In the livers of 24h-starved galactosamine-treated rats there were large increases in the concentrations of alanine (3-fold), citrate (5-fold), 2-oxoglutarate (4-fold), with smaller increases in malate, glutamate and aspartate. There was a 4-fold rise in the value of the mass-action ratio of the alanine aminotransferase system in the livers of galactosamine-treated rats when compared to controls. 5. There was a significant decrease in the activities of aspartate and alanine aminotransferases in the cytoplasm and the soluble fraction of sonicated homogenates of the livers of rats treated with galactosamine. The activity of phosphoenolpyruvate carboxylase was decreased by 75% of the control value. 6. Glucose synthesis from lactate in perfused livers from galactosamine-treated rats was inhibited 39% when compared with controls. 7. The results indicate that the conversion of lactate into glucose is decreased in the livers of galactosamine-treated rats and that this decrease may be due to the loss of phosphoenolpyruvate carboxylase from damaged hepatocytes.
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PMID:Metabolic studies in experimental liver disease resulting from D(+)-galactosamine administration. 465 44

Thymectomized DBA/2 mice, irradiated with 720 rad/min and reconstituted with syngeneic bone marrow, were treated i.p. with 1 g/kg body weight D-galactosamine-HCl (DGA). Light and electron microscopic changes characteristic of the toxic effect of the agent, such as hepatocellular cytoplasmic inclusions and unicellular necrosis, could be observed but no inflammatory reaction was detectable in the liver. The phagocytic activity of Kupffer cells proved to be unchanged in immunosuppressed animals. Liver regeneration following DGA injury took place in 120 hours exactly as in animals having an intact immune system. The experiments suggested that T-lymphocytes participate in the development of DGA-hepatitis and their absence does not influence the restoration of liver injury. The experimental system described seems to be suitable for separating primary and secondary events and also for studying the role of the immune system in toxic liver injury.
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PMID:D-galactosamine-induced liver injury in immunosuppressed mice. 608 23

After the administration of D-galactosamine to golden Syrian hamsters, a rapid but short-lived increase in acylase I and cobalt-activated (AA-Co) activity was noted in the blood plasma, but not in the liver. In the plasma of control hamsters, only form 2 AA-Co was identified, but during experimental hepatitis, the appearance of form 1 was observed. Only form 2 hamster enzyme is strongly inhibited by alpha-hydroxyisocaproil-tyrosine and reacts with antihuman form 2 antibody.
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PMID:Acylases in plasma of hamsters with experimental hepatitis. 612 85

Diethyldithiocarbamate influences galactosamine induced hepatitis in the rat. Experimental liver damage produced by galactosamine is less severe when diethyldithiocarbamate is given before or after galactosamine application. Galactosamine induced hepatitis is nearly completely suppressed when diethyldithiocarbamate is applied 24 h after galactosamine administration.
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PMID:[Protective and curative effects of diethyldithiocarbamate on galactosamine hepatitis in the rat (author's transl)]. 624 30

1. Acute galactosamine (Gal) hepatitis was induced in rats drinking ad libitum either sodic bicarbonated water of Vichy Grande Grille (GG) or ordinary tap water (OH2). Two series of experiments were performed. 2. In the first series, Gal-induced hepatitis was moderate. Twenty four hours after IP Gal injection, GG treated rats had relative to OH2 treated rats a decrease of bile flow and BSP excretion, and an increase of serum transaminase and bilirubin. Seven days after Gal the liver had returned to normal except for an increase in biliary bilirubin and liver total lipids. 3. In the second series, Gal-induced hepatitis was severe. Twenty four hours after galactosamine administration, an increase in mortality after anesthesia was found in Gal/GG rats. An increase of liver size and total hepatic lipids was also observed, while bile secretion, BSP excretion, cyt P 450 and ARN decreased in Gal/GG rats. Steatosis and inflammatory reactions were more important in Gal/GG than in Gal/OH2 rats. Most parameters came back to their normal levels in two days in Gal/OH2 rats, while 7 days were generally necessary in Gal/GG treated animals. Hepatic DNA kept increasing in Gal/GG animals and was still higher after 7 days, maybe due to a greater inflammatory reaction in the liver, maybe following a stimulated hepatocyte regenerative response. 4. These results indicate that GG water is not an inoffensive salt solution.
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PMID:[Aggravation of acute galactosamine hepatitis by a sodic bicarbonated water in rats (author's transl)]. 626 Oct 45

After application of D-galactosamine a hepatitis develops in the rat liver. This can be prevented by different agents, including tryptophan. Yet it has not been possible to give definitive conclusions about the mechanism of galactosamine hepatitis. In this paper we report about the influence of galactosamine on the NAD metabolism. D-galactosamine inhibits the NAD synthesis initiated by nicotinamide in normal and adrenalectomized animals. The NAD synthesis from tryptophan is prevented in normal animals, in adrenalectomized ones however there is an increase of NAD in the presence of D-galactosamine reduces the activity of the ADPR transferase. Inhibitors of the ADPR transferase prevent the galactosamine hepatitis. From the results presented we conclude that the ADPR transferase plays an important role in the development of the galactosamine hepatitis.
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PMID:Influence of D-galactosamine upon the NAD-metabolism in rat liver. 631 40

Permeability of the blood brain barrier in relation to the development of hepatic encephalopathy was investigated in two animal models of acute hepatic failure, in one of which there was the potential for recovery (D-galactosamine-induced hepatitis). In both this and the hepatic devascularization model, there was an approximate 3-fold increase in the passive permeability of the blood brain barrier to inulin and sucrose. Transport of amino acids was also significantly affected, with approximate 30% increases in the brain uptake of phenylalanine, tyrosine and arginine and a 65% increase in uptake of leucine. These changes are attributed to the action of circulating toxic substances, some of which increase blood brain barrier permeability in normal animals.
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PMID:Experimental studies of blood brain barrier permeability in acute hepatic failure. 637 48

After administration of D-galactosamine-HCl alterations in liver cells - histologically resembling hepatitis - occur. During this process several biochemical changes are demonstrable. The formation of these alterations may be prevented by combined administration of nicotinamide + L-methionine or DL-tryptophan + L-methionine. This had been confirmed by histology as well as by determination of GOT and GPT activity in the serum.
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PMID:The influence of nicotinamide, tryptophan, and methionine upon galactosamine-induced effects in the liver. 645 26


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