Immunochemical Detection of Lipid Hydroperoxide- and Aldehyde-Modified Proteins in Diseases

Sugiyama, Akihiko; Sun, Jinyuan

doi:10.1007/978-94-007-7920-4_10

Cited by 19 publications

(14 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The association between oxidative stress, lipid peroxidation and neurodegeneration has long been appreciated. Notably, elevated levels of lipid peroxidation are reliably detected in brain tissues and body fluids of Alzheimer’s, Parkinson’s, Huntington’s disease, motor neuron disease and multiple sclerosis patients ( Adibhatla and Hatcher, 2010 ; Shichiri, 2014 ; Sugiyama and Sun, 2014 ; Wang et al, 2014 ; Bradley-Whitman and Lovell, 2015 ). Iron accumulation is a consistent feature of neurodegeneration ( Belaidi and Bush, 2016 ).…”

Section: Evidence For Ferroptosis In Neurodegenerationmentioning

confidence: 99%

Targeting Nrf2 to Suppress Ferroptosis and Mitochondrial Dysfunction in Neurodegeneration

et al. 2018

View full text Add to dashboard Cite

Ferroptosis is a newly described form of regulated cell death, distinct from apoptosis, necroptosis and other forms of cell death. Ferroptosis is induced by disruption of glutathione synthesis or inhibition of glutathione peroxidase 4, exacerbated by iron, and prevented by radical scavengers such as ferrostatin-1, liproxstatin-1, and endogenous vitamin E. Ferroptosis terminates with mitochondrial dysfunction and toxic lipid peroxidation. Although conclusive identification of ferroptosis in vivo is challenging, several salient and very well established features of neurodegenerative diseases are consistent with ferroptosis, including lipid peroxidation, mitochondrial disruption and iron dysregulation. Accordingly, interest in the role of ferroptosis in neurodegeneration is escalating and specific evidence is rapidly emerging. One aspect that has thus far received little attention is the antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2). This transcription factor regulates hundreds of genes, of which many are either directly or indirectly involved in modulating ferroptosis, including metabolism of glutathione, iron and lipids, and mitochondrial function. This potentially positions Nrf2 as a key deterministic component modulating the onset and outcomes of ferroptotic stress. The minimal direct evidence currently available is consistent with this and indicates that Nrf2 may be critical for protection against ferroptosis. In contrast, abundant evidence demonstrates that enhancing Nrf2 signaling is potently neuroprotective in models of neurodegeneration, although the exact mechanism by which this is achieved is unclear. Further studies are required to determine to extent to which the neuroprotective effects of Nrf2 activation involve the prevention of ferroptosis.

show abstract

Section: Evidence For Ferroptosis In Neurodegenerationmentioning

confidence: 99%

Targeting Nrf2 to Suppress Ferroptosis and Mitochondrial Dysfunction in Neurodegeneration

et al. 2018

View full text Add to dashboard Cite

show abstract

“…As a result, these products are currently suggested to contribute to neurodegeneration. In addition, immunochemical detection of lipid hydroperoxide- and aldehyde-modified proteins, and selective protein targets of aldehydes were found in AD [ 23 , 24 ]. Nevertheless, relationships between lipid peroxidation products and key clinical AD features remain to be confirmed.…”

Section: Relevance Of Lipid Peroxidation Products In Neurodegeneramentioning

confidence: 99%

Isoprostanoids in Clinical and Experimental Neurological Disease Models

et al. 2018

View full text Add to dashboard Cite

Isoprostanoids are a large family of compounds derived from non-enzymatic oxidation of polyunsaturated fatty acids (PUFAs). Unlike other oxidative stress biomarkers, they provide unique information on the precursor of the targeted PUFA. Although they were discovered about a quarter of century ago, the knowledge on the role of key isoprostanoids in the pathogenesis of experimental and human disease models remains limited. This is mainly due to the limited availability of highly purified molecules to be used as a reference standard in the identification of biological samples. The accurate knowledge on their biological relevance is the critical step that could be translated from some mere technical/industrial advances into a reliable biological disease marker which is helpful in deciphering the oxidative stress puzzle related to neurological disorders. Recent research indicates the value of isoprostanoids in predicting the clinical presentation and evolution of the neurological diseases. This review focuses on the relevance of isoprostanoids as mediators and potential biomarkers in neurological diseases, a heterogeneous family ranging from rare brain diseases to major health conditions that could have worldwide socioeconomic impact in the health sector. The current challenge is to identify the preferential biochemical pathways that actually follow the oxidative reactions in the neurological diseases and the consequence of the specific isoprostanes in the underlying pathogenic mechanisms.

show abstract

“…Lipid peroxidation can generate unsaturated aldehydes, which are the signaling molecules of the mitochondria. Lipid peroxidation may also activate cell apoptosis pathways, such as Fas/FasL, to induce cell apoptosis ( 25 ). Biologically active α,β-unsaturated aldehydes can be used to detect effects on glioma after development of an appropriate glioma mitochondria model.…”

Section: Discussionmentioning

confidence: 99%

Effect of lithocholic acid on biologically active α,β-unsaturated aldehydes induced by H2O2 in glioma mitochondria for use in glioma treatment

Wang

Bie

et al. 2018

Int J Mol Med

View full text Add to dashboard Cite

Lithocholic acid (LCA) is known to kill glioma cells while sparing normal neuronal cells. However, the anti-glioma mechanism of LCA is unclear at present. Although malondialdehyde (MDA) is not specific to detect tumors, biologically active α,β-unsaturated aldehydes can be used to detect the outcome of gliomas, especially the mitochondria, as a research tool. The purpose of this research was to determine the optimum conditions for a lipid peroxidation model, according to changes in the aldehydes formed from the reaction between 2-thiobarbituric acid and biologically active α,β-unsaturated aldehydes. Experimental methods and procedures were successfully established for a model of lipid peroxidation induced by H2O2 in glioma mitochondria for glioma treatment and optimum conditions for LCA treatment were determined. The optimal conditions for the model were a glioma mitochondrial concentration of 1.5 mg/ml, H2O2 concentration of 0.3 mg/ml, duration of action of 30 min, and addition of 4.0 ml of 46 mM thiobarbituric acid. The effect of LCA, as determined by changes in the UV peaks at 450, 495, and 532 nm, was optimal at a concentration of 100 µM, a duration of action of 15 min, and in an acidic microenvironment. The study concluded that a suitable concentration of LCA has anti-glioma effects as determined by the effect on changes in the UV peaks at 450, 495 and 532 nm and the mitochondrial model developed should be conducive to further in-depth research.

show abstract

Immunochemical Detection of Lipid Hydroperoxide- and Aldehyde-Modified Proteins in Diseases

Cited by 19 publications

References 63 publications

Targeting Nrf2 to Suppress Ferroptosis and Mitochondrial Dysfunction in Neurodegeneration

Targeting Nrf2 to Suppress Ferroptosis and Mitochondrial Dysfunction in Neurodegeneration

Isoprostanoids in Clinical and Experimental Neurological Disease Models

Effect of lithocholic acid on biologically active α,β-unsaturated aldehydes induced by H2O2 in glioma mitochondria for use in glioma treatment

Contact Info

Product

Resources

About