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《Free radical research》2013,47(12):1066-1075
Abstract3-Hydroxy-3-methylglutaryl-CoA lyase (HL) deficiency is a disorder biochemically characterized by the predominant accumulation of 3-hydroxy-3-methylglutarate (HMG), 3-methylglutarate (MGA), 3-methylglutaconate and 3-hydroxyisovalerate in tissues and biological fluids of the affected patients. Neurological symptoms and hepatopathy are commonly found in HL deficiency, especially during metabolic crises. Since the mechanisms of tissue damage in this disorder are not well understood, in the present study we evaluated the ex vivo effects of acute administration of HMG and MGA on important parameters of oxidative stress in cerebral cortex and liver from young rats. In vivo administration of HMG and MGA provoked an increase of carbonyl and carboxy-methyl-lysine formation in cerebral cortex, but not in liver, indicating that these metabolites induce protein oxidative damage in the brain. We also verified that HMG and MGA significantly decreased glutathione concentrations in both cerebral cortex and liver, implying a reduction of antioxidant defenses. Furthermore, HMG and MGA increased 2’,7’-dichlorofluorescin oxidation, but did not alter nitrate and nitrite content in cerebral cortex and liver, indicating that HMG and MGA effects are mainly mediated by reactive oxygen species. HMG and MGA also increased the activities of superoxide dismutase and catalase in cerebral cortex and liver, whereas MGA decreased glutathione peroxidase activity in cerebral cortex. Our present data showing a disruption of redox homeostasis in cerebral cortex and liver caused by in vivo administration of HMG and MGA suggest that this pathomechanism may possibly contribute to the brain and liver abnormalities observed in HL-deficient patients. 相似文献
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Phillip?David?Whitfield Peter-John?Mantyla?Noble Hilary?Major Robert?Jeffrey?Beynon Rachel?Burrow Alistair?Iain?Freeman Alexander?James?GermanEmail author 《Metabolomics : Official journal of the Metabolomic Society》2005,1(3):215-225
Human hepatopathies are a diagnostic challenge, with many distinct diseases having similar clinical signs and laboratory findings.
Naturally occurring canine hepatic disease provides an excellent model for human diseases and similar diagnostic dilemmas
exist; differentiating canine congenital portosystemic vascular anomalies (PVA) from acquired hepatopathies is difficult and
traditionally requires invasive diagnostic procedures. The emerging post-genomic science of metabolomics is concerned with
detecting global changes of populations of endogenous low molecular weight metabolites in biological samples and offers the
possibility of identifying surrogate profiles of disease. Metabolomics couples sensitive metabolite analysis with sophisticated
pattern recognition techniques. In this study, a metabolomic strategy has been employed to assess metabolite changes in the
plasma of dogs with congenital PVA and acquired hepatic disease. Plasma samples were collected from 25 dogs, comprising 9
dogs with congenital PVA, 6 with acquired hepatopathy and 10 with non-hepatic disorders. Low molecular weight metabolites
were analyzed by liquid chromatography-mass spectrometry (LC-MS). Following identification of metabolites, multivariate data
analysis was used to compare profiles amongst groups. The analysis demonstrated significant disturbances in the plasma bile
acid and phospholipid profiles of dogs with portovascular anomalies. In contrast to traditional laboratory parameters, the
metabolomic strategy was able to produce a clear segregation between all three study groups. In conclusion, this study demonstrates
the potential of metabolomics as a diagnostic tool for naturally occurring hepatic disease. With further validation, this
approach will improve diagnostic capabilities, provide an insight into pathogenetic mechanisms, and ultimately inform therapeutic
decision making in clinical hepatology.
This work was supported in part by grants from The Royal Society, Petplan Charitable Trust and The Waltham Foundation. 相似文献
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Hepatocellular carcinoma in a free‐living marmoset (Callithrix sp.) with concomitant biliary trematodiasis 下载免费PDF全文
J. Díaz‐Delgado T. C. Sanches C. dos Santos‐Cirqueira A. A. C. Coimbra J. M. Guerra A. Joppert C. Di Loretto M. B. Rizardi M. Sansone F. O. Nagamori P. S. Gonçalves R. Ressio S. Iglezias N. C. C. A. Fernandes C. Kanamura K. R. Groch J. L. Catão‐Dias 《Journal of medical primatology》2018,47(2):128-131
Hepatocellular carcinoma (HCC) is rare in New World primates. We report the gross, microscopical, and immunocytochemical features of a spontaneous HCC in a free‐living marmoset (Callithrix sp.). Hepatitis B and C virus and aflatoxin immunohistochemistry were negative; however, concomitant intra‐ and extrahepatic biliary trematodiasis could have played a role. 相似文献
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We studied the effects of a single post whole-body low-dose irradiation (50 cGy of γ-ray) on mice with ferric nitrilotriacetate (Fe3+-NTA)-induced transient hepatopathy. As a result, low-dose irradiation accelerated the rate of recovery. Based on the changes in glutamic oxaloacetic transaminase (GOT) activities, glutamic pyruvic transaminase (GPT) activities and lipid peroxide levels, it was shown that hepatopathy was improved by low-dose irradiation 3 h after Fe3+-NTA administration. This may be because of the enhancement of antioxidant agents such as total glutathione (GSH + GSSG), glutathione peroxidase (GPX), glutathione reductase (GR) and γ-glutamylcysteine synthetase (γ-GCS) by low-dose irradiation. These findings suggest that low-dose irradiation relieved functional disorders at least in the livers of mice with active oxygen species related diseases. 相似文献
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Shlosberg Alan Elkin Nathan Malkinson Mertyn Orgad Uri Hanji Vera Bogin Eitan Weisman Yoram Meroz Michael Bock Rachel 《Mycopathologia》1997,138(2):71-76
The feeding of a shipment of imported corn was associated with a severe reduction in growth and increased mortality in geese,
and increased mortality in broilers. Pathological examinations revealed hepatopathy, visceral gout and mild nephropathy in
geese, and in broilers an hepatopathy, which was often severe, and ascites. Samples of feed from affected geese farms were
examined for up to 24 mycotoxins, and ochratoxin was found in 6 of 15 samples at levels up to 930 ng/g. The syndrome was experimentally
reproduced by feeding geese and broilers suspect feeds with the natural ochratoxin contamination. It is believed that another,
unidentified, mycotoxin was the major cause of the hepatotoxicity, and that ochratoxin served in this case as an indicator
of a multi-mycotoxin involvement.
This revised version was published online in June 2006 with corrections to the Cover Date. 相似文献
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