Alterations of 3-nitrotyrosine concentration in the cerebrospinal fluid during aging and in patients with Alzheimer's disease

Tohgi, Hideo; Abe, Takashi; Yamazaki, Kazuma; Murata, Tetsuya; Ishizaki, Eri; Isobe, Chiaki

doi:10.1016/s0304-3940(99)00406-1

Cited by 156 publications

(96 citation statements)

References 23 publications

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“…35,42 Here we report that nanoceria reduced in situ ROS/RNS, as visualized by decreasing APF oxidation ( Figure 2) and 3-nitrotyrosine (3-NT) nitration in both SNOC and Ab [25][26][27][28][29][30][31][32][33][34][35] stressed neurons (Figures 3a-c). This is important because increased levels of nitrated proteins have been reported in AD brains and cerebrospinal fluid of AD patients, 43 and numerous proteins in AD have been shown to be nitrated by peroxynitrite. 44 For example, peroxisome proliferator-activated receptor gamma expression protects neurons from Abmediated toxicity; 45 however, its nitration prevents its translocation to the nucleus, thereby preventing mitochondrial biogenesis.…”

Section: Discussionmentioning

confidence: 99%

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

et al. 2014

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Evidence indicates that nitrosative stress and mitochondrial dysfunction participate in the pathogenesis of Alzheimer's disease (AD). Amyloid beta (Ab) and peroxynitrite induce mitochondrial fragmentation and neuronal cell death by abnormal activation of dynamin-related protein 1 (DRP1), a large GTPase that regulates mitochondrial fission. The exact mechanisms of mitochondrial fragmentation and DRP1 overactivation in AD remain unknown; however, DRP1 serine 616 (S616) phosphorylation is likely involved. Although it is clear that nitrosative stress caused by peroxynitrite has a role in AD, effective antioxidant therapies are lacking. Cerium oxide nanoparticles, or nanoceria, switch between their Ce 3 þ and Ce 4 þ states and are able to scavenge superoxide anions, hydrogen peroxide and peroxynitrite. Therefore, nanoceria might protect against neurodegeneration. Here we report that nanoceria are internalized by neurons and accumulate at the mitochondrial outer membrane and plasma membrane. Furthermore, nanoceria reduce levels of reactive nitrogen species and protein tyrosine nitration in neurons exposed to peroxynitrite. Importantly, nanoceria reduce endogenous peroxynitrite and Ab-induced mitochondrial fragmentation, DRP1 S616 hyperphosphorylation and neuronal cell death.

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Section: Discussionmentioning

confidence: 99%

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

et al. 2014

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“…have been described in brain, cerebrospinal fluid (CSF), blood, and/or urine of AD patients (8,9). Epidemiological studies have demonstrated an association between dietary antioxidant consumption and a lowered risk for the development of AD (10) although not all have confirmed this observation (11).…”

Section: Congo Redmentioning

confidence: 99%

A Potential Role of the Curry Spice Curcumin in Alzheimers Disease

Ringman¹,

Frautschy²,

Cole³

et al. 2005

CAR

440

281

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There is substantial in-vitro data indicating that curcumin has antioxidant, anti-inflammatory, and anti-amyloid activity. In addition, studies in animal models of Alzheimer's disease (AD) indicate a direct effect of curcumin in decreasing the amyloid pathology of AD. As the widespread use of curcumin as a food additive and relatively small shortterm studies in humans suggest safety, curcumin is a promising agent in the treatment and/or prevention of AD. Nonetheless, important information regarding curcumin bioavailability, safety and tolerability, particularly in an elderly population is lacking. We are therefore performing a study of curcumin in patients with AD to gather this information in addition to data on the effect of curcumin on biomarkers of AD pathology.

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“…For example, in neurodegenerative illnesses such as Alzheimer's disease, it is established that 3-NT levels increase in the brain, especially in disease-associated plaques (Smith et al, 1997;Tohgi et al, 1999), yet it is uncertain whether protein nitration is a cause or effect of the disease process. To understand how tyrosine nitration may contribute to Alzheimer's disease pathogenesis, one would need to identify the particular proteins that become nitrated, specify their sites of nitration, and elucidate the functional consequences of this modification.…”

Section: Beyond Quantification: Specification Of 3-nt Sites In Proteinsmentioning

confidence: 99%

Protein 3-Nitrotyrosine in Complex Biological Samples: Quantification by High-Pressure Liquid Chromatography/Electrochemical Detection and Emergence of Proteomic Approaches for Unbiased Identification of Modification Sites

Nuriel

Deeb

Hajjar

et al. 2008

Methods in Enzymology

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Nitration of tyrosine residues by nitric oxide (NO)-derived species results in the accumulation of 3-nitrotyrosine in proteins, a hallmark of nitrosative stress in cells and tissues. Tyrosine nitration is recognized as one of the multiple signaling modalities used by NO-derived species for the regulation of protein structure and function in health and disease. Various methods have been described for the quantification of protein 3-nitrotyrosine residues, and several strategies have been presented toward the goal of proteome-wide identification of protein tyrosine modification sites. This chapter details a useful protocol for the quantification of 3-nitrotyrosine in cells and tissues using high-pressure liquid chromatography with electrochemical detection. Additionally, this chapter describes a novel biotin-tagging strategy for specific enrichment of 3-nitrotyrosine-containing peptides. Application of this strategy, in conjunction with high-throughput MS/MS-based peptide sequencing, is anticipated to fuel efforts in developing comprehensive inventories of nitrosative stress-induced protein-tyrosine modification sites in cells and tissues.

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Alterations of 3-nitrotyrosine concentration in the cerebrospinal fluid during aging and in patients with Alzheimer's disease

Cited by 156 publications

References 23 publications

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

A Potential Role of the Curry Spice Curcumin in Alzheimers Disease

Protein 3-Nitrotyrosine in Complex Biological Samples: Quantification by High-Pressure Liquid Chromatography/Electrochemical Detection and Emergence of Proteomic Approaches for Unbiased Identification of Modification Sites

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