http://www.cnr.it/ontology/cnr/individuo/prodotto/ID217077
Oxidative stress in fulminant hepatic failure: Comparison of two pig models with and without liver necrosis (Articolo in rivista)
- Type
- Label
- Oxidative stress in fulminant hepatic failure: Comparison of two pig models with and without liver necrosis (Articolo in rivista) (literal)
- Anno
- 2001-01-01T00:00:00+01:00 (literal)
- Alternative label
Kusmic C, Boggi U, Bellini R, Vistoli F, Castellari M, Taddei G, Minervini A, Filipponi F, Mosca F, Barsacchi R (2001)
Oxidative stress in fulminant hepatic failure: Comparison of two pig models with and without liver necrosis
in Hepato-gastroenterology
(literal)
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- Kusmic C, Boggi U, Bellini R, Vistoli F, Castellari M, Taddei G, Minervini A, Filipponi F, Mosca F, Barsacchi R (literal)
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- Note
- ISI Web of Science (WOS) (literal)
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- [1] CNR, Ist Fisiol Clin, I-56127 Pisa, Italy
[2 ] Univ Pisa, Dept Oncol, Div Gen Surg, Pisa, Italy
[3] Univ Pisa, Dept Physiol & Biochem, Pisa, Italy (literal)
- Titolo
- Oxidative stress in fulminant hepatic failure: Comparison of two pig models with and without liver necrosis (literal)
- Abstract
- demonstrated how liver necrosis worsens the evolution of fulminant hepatic failure. Considering that several types of liver injury are associated with oxidative stress, we decided to measure plasma oxidative markers in two pig models of fulminant hepatic failure without and with liver necrosis.
Methodology:: Fulminant hepatic failure was produced in two groups of six pigs each by either total hepatectomy or complete hepatic devascularization.) The following parameters were recorded before and during the course of hepatic failure: electrocerebral activity, plasma vitamin E, malondialdehyde and fluorescent protein-aldehyde adducts, total cholesterol, lactate-dehydrogenase, creatine phosphokinase, and ammonium.
Results: Despite comparable survival periods, hepatic necrosis was associated with earlier electrocerebral deterioration. Plasma concentration of malondialdehyde and fluorescent protein-aldehyde adducts rose and vitamin E content decreased in both groups. However, while in the group without liver necrosis the rates of cholesterol and vitamin E decay were identical, in the group with liver necrosis cholesterol concentration decreased less than vitamin E concentration, strongly indicating a true intravascular oxidation of vitamin E. Interestingly, in both models the rise of oxidative parameters preceded the development of cell injury.
Conclusions: Oxidative stress, although present in both models, was significantly higher in the group with Liver necrosis. (literal)
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