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Target Concepts:
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Query: EC:2.6.1.1 (
aspartate aminotransferase
)
21,665
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Mice infected with
Schistosoma mansoni
were highly sensitive to the lethal effects of bacterial lipopolysaccharide (LPS). The hyper-reactive state of LPS coincided with the development around the parasite eggs of multiple granulomas in the liver. Elevated
aspartate transaminase
levels in blood and severe hypoglycaemia in LPS-challenged animals indicated extensive liver parenchymal cell damage. There was also a complete depletion of glycogen in hepatocytes of these animals. From this work and studies on other hepatitis models, it is suggested that individuals affected with granulomatous disorders may be at risk because of everyday exposure to LPS from the gut.
...
PMID:Increased hepatotoxicity of bacterial lipopolysaccharide in mice infected with Schistosoma mansoni. 55 82
Patients infected with
Schistosoma mansoni
showed an abnormal response to a test dose of tryptophan, with little increase in the urinary excretion of kynurenine, hydroxykynurenine, xanthurenic and kynurenic acids, N1-methyl nicotinamide, methyl pyridone carboxamide, 5-hydroxytryptamine or 5-hydroxyindoleacetic acid. In contrast to previous reports, this is different from the pattern of tryptophan metabolism seen in vitamin B6 deficiency. Furthermore, the patients' plasma concentrations of pyridoxal phosphate were within the reference range, and supplementation for 5 days with 20 mg vitamin B6/day did not affect tryptophan metabolism. Treatment with a single dose of Praziquantel resulted in a substantial restoration of normal tryptophan metabolism. In mice infected with S. mansoni there was a similar impairment of tryptophan metabolism, as shown by considerably reduced formation of 14CO2 after the administration of a tracer dose of [14C]tryptophan. Again, the administration of vitamin B6 supplements did not correct tryptophan metabolism in the mice. Treatment with Praziquantel resulted in substantial restoration of the production of 14CO2 from [14C]tryptophan. There was no evidence of vitamin B6 deficiency (as determined by erythrocyte
aspartate aminotransferase
activation coefficient) associated with infection in the mice, although there was a redistribution of pyridoxal phosphate between tissues, with a reduction in the concentration of liver, spleen and kidney, and an increase in skeletal muscle.
...
PMID:Tryptophan metabolism and vitamin B6 nutritional status in patients with schistosomiasis mansoni and in infected mice. 164 Dec 43
In mice, infection with 20-30 cercariae of
Schistosoma mansoni
resulted in a considerable reduction in the formation of 14CO2 from [14C]tryptophan. Infected animals excreted significantly lower amounts of kynurenine, kynurenic acid, and methyl pyridone carboxamide than did uninfected controls. There was no difference in the ability of hepatocytes isolated from infected or control animals to metabolise [14C]tryptophan. Hepatocytes from infected animals synthesized less NAD(P), but more niacin and N1-methyl nicotinamide from tryptophan. They showed no greater accumulation of kynurenine metabolites than did cells from control animals. The hepatocyte content of pyridoxal phosphate and the erythrocyte
aspartate aminotransferase
activation coefficient were the same in both groups of mice, suggesting that infection with S. mansoni does not deplete vitamin B6. The impairment of tryptophan metabolism in vivo was apparently not due to impaired hepatic metabolism. Rather, it seems likely that the parasites or their eggs take up tryptophan avidly from the host's circulation. Studies of parasite and egg metabolism of tryptophan may suggest novel approaches to the chemotherapy of bilharzia.
...
PMID:Schistosoma mansoni: effects on tryptophan metabolism in mice. 213 33
The activities of
aspartate aminotransferase
(
AST
) (EC.2.6.1.1.) I, alanine aminotransferase (ALT) (EC.2.6.1.2) II and lactate dehydrogenase (LD) (EC.1.1.1.27) III have been measured in tissue homogenate and in haemolymph of Biomphalaria alexandrina snails, the specific intermediate host for the human parasitic disease schistosomiasis due to
Schistosoma mansoni
.
...
PMID:Selected enzymatic activities in fresh water snails, specific intermediate host for human schistosomiasis. 249 22
Cholylglycine levels were measured by radioimmunoassay in sera from 10 control CFI female mice and 22 CFI female mice experimentally infected with
Schistosoma mansoni
. Cholylglycine was significantly elevated in sera of all but one of the chronically infected animals. Serum
aspartate transaminase
was within normal limits in all the infected animals; while five infected mice had elevated serum alkaline phosphatase and all these five also had high levels of serum cholylglycine. Marked hepatic histopathological changes were demonstrated in all the infected animals. The data suggest that serum cholylglycine is a highly sensitive index for hepatic dysfunction in chronic hepatic schistosomiasis mansoni.
...
PMID:Radioimmunoassay of serum conjugated cholic acid in hepatic murine schistosomiasis. 653 47
From this comparison of 37 black children with hepatic schistosomiasis (HS) and 53 with intestinal
Schistosoma mansoni
(IS) living in an endemic area, we propose easily identifiable clinical features of mild HS. These patients were generally well nourished school-age children who seldom complained of dysentery but who had a firm hepatomegaly with predominant enlargement of the left lobe and a firm splenomegaly. They were also mildly anaemic (9.4 +/- 2.2 g/dl) and had low serum albumin (30 +/- 7 g/l), raised
aspartate transaminase
(36 +/- 31 u/l) and high globulins (53 +/- 15 g/l). The implications of the absence of severe hepatosplenic schistosomiasis in many of these children are discussed.
...
PMID:Clinical recognition of mild hepatic schistosomiasis in an endemic area. 671 May 66
Colchicine in a dose of 200 micrograms kg body weight/day (5 days/week) was administered to groups of
Schistosoma mansoni
infected mice 12 weeks post infection, either alone or following previous praziquantel therapy at the 8th week of infection. Certain groups received colchicine for 6 weeks and others received it for 10 weeks. Colchicine alone did not significantly change the light microscopic appearance of schistosomal liver fibrosis, or hepatic collagen content estimated histomorphometrically, and did not reduce the elevated IL-2 serum level. Colchicine induced hepatic injury consisted of intense inflammatory reaction in granuloma and portal tracts, hepatocytic degeneration, and elevation of serum
AST
and ALT levels. Colchicine seemed to postpone granulomatous reaction healing and collagen deposition rather than inhibiting collagen formation or degrading it. Colchicine inhibited proliferation of hepatocytes of infected mice by expanding G2-M phases of cell cycle, thus reduced Ag NOR count and raised cell ploidy and cyclic AMP serum level. Subsidence of schistosomal infection by praziquantel prior to colchicine therapy greatly reduced inflammatory cellular reaction, significantly diminished hepatic collagen deposition and serum IL-2 level, minimized the elevated nuclear ploidy and cyclic AMP serum level that followed colchicine therapy when administered alone.
...
PMID:Colchicine therapy for hepatic murine schistosomal fibrosis: image analysis and serological study. 1036 84
We tested the ability of carnosine to improve some liver disorders induced by
Schistosoma mansoni
parasite in hamsters (Mesocricetus auratus). Results indicate that parasitic infestation induced elevation in serum alkaline phosphatase, gamma-glutamyl transferase,
aspartate aminotransferase
and procollagen III peptide as a marker of liver fibrosis. Administration of carnosine (10 mg/day) for 15 days either concurrent with infection, 2 and 4 weeks post-infestation was effective in reducing differential worm burden. It was also effective in renormalizing blood glucose level depending on the time course. The most evident effect of carnosine was on serum procollagen III peptide level, which was lowered in infested groups treated with carnosine. Histopathological studies confirmed the potential use of carnosine for intervention in schistosomiasis.
...
PMID:Effects of carnosine on bilharzial infestation in hamsters: biochemical and histochemical studies. 1195 36
DNA microsatellites were used as molecular markers to analyse the population structure of the laboratory LE strain and of 10 field isolates of
Schistosoma mansoni
, the aetiologic agent of schistosomiasis. Out of 16,000 DNA sequences analysed in databases, 622 microsatellite loci were identified in 481 sequences (3.0%). The AT repetitions were the most frequent, followed by
AAT
and AC. Six loci showing perfect repetitions were selected and used in the polymerase chain reaction to evaluate polymorphisms in the number of repeats. Two groups of worms were studied. The first group consisted of 78 individuals, 39 of each sex, of the LE strain. The second group of worms consisted of 10 field isolates: seven from humans and three from snails. Four of the six loci were polymorphic, containing 11-17 alleles per locus. No linkage disequilibrium was observed among loci and none of the loci was sex linked. In both groups of worms, a significant deviation from Hardy-Weinberg equilibrium was observed. The observed heterozygosity was always lower than the expected one. The polymerase chain reaction primers were S. mansoni specific. The LE strain showed a lower total number of alleles or a lower average number of alleles/polymorphic locus than the field isolates, suggesting that 41 years of laboratory maintenance exerted selective pressure on the LE strain. The S. mansoni populations from the field were most genetically undifferentiated (R(ST)<0.027), suggesting a high gene flow among them. Our results showed the usefulness of microsatellites for population analysis of S. mansoni, offering a new alternative for a better understanding of schistosomiasis epidemiology.
...
PMID:Populational structure of Schistosoma mansoni assessed by DNA microsatellites. 1206 55
To investigate whether infection with human immunodeficiency virus 1 (HIV-1) affects fibrosis development in patients infected with
Schistosoma mansoni
, we evaluated schistosomiasis-induced pathology in the livers of Kenyan patients co-infected with HIV-1. Compared with persons with schistosomiasis alone (n = 58), there were no significant differences in distribution of ultrasound-detectable pathology in persons with HIV-1 co-infection (n = 23). Similarly, serum
aspartate aminotransferase
levels were not significantly different in HIV-1+ individuals. Hepatic fibrosis was associated with significantly decreased CD4+ T cell counts, even in the absence of HIV-1 infection. These data suggest that HIV-1 co-infection does not significantly alter the proportion of patients experiencing schistosomiasis-induced fibrosis, but pathology associated with S. mansoni infections leads to CD4+ T cell reductions and thereby may exacerbate the effects of HIV-1 in co-infected individuals.
...
PMID:Short report: Evaluation of hepatic fibrosis in persons co-infected with Schistosoma mansoni and human immunodeficiency virus 1. 1564 72
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