2005
DOI: 10.1016/j.febslet.2005.08.085
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The relation between sphingomyelinase activity, lipid peroxide oxidation and NO‐releasing in mice liver and brain

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 a (TNF-a). We found that ceramide can induce peroxide oxidation and lead to accumulation of TNF-a in animal organs. Nitric oxide (NO) donors (S-nitrosoglutath… Show more

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Cited by 19 publications
(10 citation statements)
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“…Exercise training has been shown to reduce plasma inflammatory markers including tumor necrosis factor[78], a key inducer of ceramide synthesis[86]. Reduced inflammatory signaling with exercise has been associated with decreased de novo synthesis of ceramides[87].…”
Section: Discussionmentioning
confidence: 99%
“…Exercise training has been shown to reduce plasma inflammatory markers including tumor necrosis factor[78], a key inducer of ceramide synthesis[86]. Reduced inflammatory signaling with exercise has been associated with decreased de novo synthesis of ceramides[87].…”
Section: Discussionmentioning
confidence: 99%
“…In addition to iron-induced lipid peroxidation, iron can also promote sphingomyelin breakdown via activation of sphingomyelinases, generating the product ceramide (which is involved in mediating the regulated cell death response) [101] that then contributes to neuronal apoptosis, a feature of neurodegenerative diseases. In support, increased levels of sphingomyelin coinciding with reduced ceramide content is associated with neuronal protection and may thus be a targetable pathway (using iron chelators) for treatment [102].…”
Section: Iron and Lipids: Neurodegenerative Diseasesmentioning
confidence: 99%
“…The process is realized at least via two mechanisms: (a) inactivation of caspases due to oxidation of their active site thiol groups; b) critical decrease of intracellular ATP con centrations due to oxidative damage of mitochondria. It is known that administration of TNF α to rats increased LPO content and nSMase activity in the brain and liver [25]. Taking into consideration these data and also lack of unified classification of severity of oxidative stress, we suggest that under our experimen tal conditions increased serum concentrations of TNF α and hepatic CD and TBARS (Table 4) may promote activation of the key enzyme of the SM cycle observed by day 3 of starvation.…”
Section: Resultsmentioning
confidence: 79%