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The relation between sphingomyelinase activity, lipid peroxide oxidation and NO‐releasing in mice liver and brain
Author(s) -
Alessenko A.V.,
Shupik M.A.,
Gutner U.A.,
Bugrova A.E.,
Dudnik L.B.,
Shingarova L.N.,
Mikoyan A.,
Vanin A.F.
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.08.085
Subject(s) - sphingomyelin , lipid peroxidation , nitric oxide , ceramide , chemistry , sphingomyelin phosphodiesterase , lipid peroxide , oxidative phosphorylation , peroxide , biochemistry , hydrogen peroxide , tumor necrosis factor alpha , oxidative stress , endocrinology , biology , cholesterol , apoptosis , organic chemistry
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 α (TNF‐α). We found that ceramide can induce peroxide oxidation and lead to accumulation of TNF‐α 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.