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FEBS Lett ; 579(25): 5571-6, 2005 Oct 24.
Article in English | MEDLINE | ID: mdl-16225875

ABSTRACT

We used animal models to study connection between oxidating system and sphingomyelin signaling cascade, because this models are more close related to people disease. Activation of n-sphingomyelinase (n-SMase) in mice liver and brain is coincided in time with increased level of peroxide products (conjugated dienes) after injection of tumor necrosis factor alpha (TNF-alpha). We found that ceramide can induce peroxide oxidation and lead to accumulation of TNF-alpha in animal organs. Nitric oxide (NO) donors (S-nitrosoglutathione and dinitrosyl iron complex) reversibly inhibited activity of n-SMase and decreased level of lipid peroxidation products. This data proposed that both SMase and messengers of oxidative systems could be targets for NO-derived oxidants.


Subject(s)
Brain/metabolism , Lipid Peroxidation , Liver/metabolism , Nitric Oxide/metabolism , Sphingomyelin Phosphodiesterase/metabolism , Animals , Brain/drug effects , Brain/enzymology , Ceramides/pharmacology , Iron/pharmacology , Lipid Peroxidation/drug effects , Liver/drug effects , Liver/enzymology , Male , Mice , Mice, Inbred BALB C , Nitrogen Oxides/pharmacology , S-Nitrosoglutathione/pharmacology , Sphingomyelin Phosphodiesterase/antagonists & inhibitors , Tumor Necrosis Factor-alpha/metabolism , Tumor Necrosis Factor-alpha/pharmacology
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