F4-neuroprostanes mediate neurological severity in Rett syndrome

Signorini, Cinzia; Felice, Claudio De; Leoncini, Silvia; Giardini, Anna; D’Esposito, Maurizio; Filosa, Stefania; Ragione, Floriana Della; Rossi, Marcello; Pecorelli, Alessandra; Valacchi, Giuseppe; Ciccoli, Lucia; Hayek, Joussef

doi:10.1016/j.cca.2011.04.016

Cited by 69 publications

(76 citation statements)

References 51 publications

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“…In addition, our fi ndings indicate the importance of plasma as a suitable biological fl uid for detecting markers of central nervous system oxidative damage in RTT ( 16,54,55 ) and underline the key role of interaction between organic chemists, OS biochemists, and clinicians in the discovery of new markers of disease and potential targets for new interventional strategies.…”

Section: Discussionmentioning

confidence: 99%

F2-dihomo-isoprostanes as potential early biomarkers of lipid oxidative damage in Rett syndrome

Felice

Signorini

Durand

et al. 2011

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 99%

F2-dihomo-isoprostanes as potential early biomarkers of lipid oxidative damage in Rett syndrome

Felice

Signorini

Durand

et al. 2011

Journal of Lipid Research

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“…In particular, high Biochimica et Biophysica Acta 1852 (2015) 2066-2074 levels of IsoPs and HNE, which are major lipid peroxidation products generated from membrane lipids by free radical reactions, are strongly associated with the disease natural history, genotype-phenotype correlation, clinical heterogeneity and severity of the disease [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Impaired enzymatic defensive activity, mitochondrial dysfunction and proteasome activation are involved in RTT cell oxidative damage

Cervellati

Sticozzi

Romani

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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A strong correlation between oxidative stress (OS) and Rett syndrome (RTT), a rare neurodevelopmental disorder affecting females in the 95% of the cases, has been well documented although the source of OS and the effect of a redox imbalance in this pathology has not been yet investigated. Using freshly isolated skin fibroblasts from RTT patients and healthy subjects, we have demonstrated in RTT cells high levels of H2O2 and HNE protein adducts. These findings correlated with the constitutive activation of NADPH-oxidase (NOX) and that was prevented by a NOX inhibitor and iron chelator pre-treatment, showing its direct involvement. In parallel, we demonstrated an increase in mitochondrial oxidant production, altered mitochondrial biogenesis and impaired proteasome activity in RTT samples. Further, we found that the key cellular defensive enzymes: glutathione peroxidase, superoxide dismutase and thioredoxin reductases activities were also significantly lower in RTT. Taken all together, our findings suggest that the systemic OS levels in RTT can be a consequence of both: increased endogenous oxidants as well as altered mitochondrial biogenesis with a decreased activity of defensive enzymes that leads to posttranslational oxidant protein modification and a proteasome activity impairment.

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“…Seet et al [36] have shown that F 4 -NeuroP plasma levels of Parkinson's disease patients were elevated when compared to controls and were independent of the severity of the disease. In addition, plasma of adolescent RTT patients had increased levels of free F 4 -NeuroPs in comparison with healthy controls, and the levels correlated with the severity of the illness [37]. Aside from neurodegenerative diseases, onset of ischemic-stroke also showed to be associated with augmented plasma concentrations of free and esterified F 4 -NeuroPs, and the levels remained high after the onset, especially for the free form [38].…”

Section: Neuroprostanes and Neurofurans As Oxidative Stress Biomarkersmentioning

confidence: 96%

“…However, contrasting outcome was found in supplementation of RTT patients with n-3 PUFA from fish oil in which plasma free F 4 -NeuroPs concentrations were lower when compared to controls. Also, the level of free F 4 -NeuroPs released was inversely associated with cardiac left ventricular systolic function in the RTT patients after fish oil supplementation [37,60,80].…”

Section: Bioactive Lipids and Potential Signaling Moleculesmentioning

confidence: 97%

Non-enzymatic cyclic oxygenated metabolites of adrenic, docosahexaenoic, eicosapentaenoic and α-linolenic acids; bioactivities and potential use as biomarkers

Galano

Lee

Gladine

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Cyclic oxygenated metabolites are formed in vivo through non-enzymatic free radical reaction of n-6 and n-3 polyunsaturated fatty acids (PUFAs) such as arachidonic (ARA C20:4 n-6), adrenic (AdA 22:4 n-6), α-linolenic (ALA 18:3 n-3), eicosapentaenoic (EPA 20:5 n-3) and docosahexaenoic (DHA 22:6 n-3) acids. These cyclic compounds are known as isoprostanes, neuroprostanes, dihomo-isoprostanes and phytoprostanes. Evidence has emerged for their use as biomarkers of oxidative stress and, more recently, the n-3PUFA-derived compounds have been shown to mediate bioactivities as secondary messengers. Accordingly, this review will focus on the cyclic oxygenated metabolites generated from AdA, ALA, EPA and DHA. This article is part of a Special Issue entitled "Oxygenated metabolism of PUFA: analysis and biological relevance".

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F4-neuroprostanes mediate neurological severity in Rett syndrome

Cited by 69 publications

References 51 publications

F2-dihomo-isoprostanes as potential early biomarkers of lipid oxidative damage in Rett syndrome

F2-dihomo-isoprostanes as potential early biomarkers of lipid oxidative damage in Rett syndrome

Impaired enzymatic defensive activity, mitochondrial dysfunction and proteasome activation are involved in RTT cell oxidative damage

Non-enzymatic cyclic oxygenated metabolites of adrenic, docosahexaenoic, eicosapentaenoic and α-linolenic acids; bioactivities and potential use as biomarkers

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