3-Nitrotyrosine: a versatile oxidative stress biomarker for major neurodegenerative diseases

Bandookwala, Maria; Sengupta, Pinaki

doi:10.1080/00207454.2020.1713776

Cited by 94 publications

(69 citation statements)

References 131 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The nitrotyrosine-modified proteins have been described in PD substantia nigra and in Lewy bodies [49,50]. Their levels, in the clinical setting, have been proposed as functional and quantitative biomarkers of oxidative/nitrosative stress, correlated to the progression of neurodegenerative lesions [50]. In this study, we also evaluated the effect of RT alone or co-incubated with CURC on the level of nitrated proteins.…”

Section: Discussionmentioning

confidence: 99%

“…Tyrosine is susceptible to nitration and oxidation, as it is often exposed at protein's surface [48]. The nitrotyrosine-modified proteins have been described in PD substantia nigra and in Lewy bodies [49,50]. Their levels, in the clinical setting, have been proposed as functional and quantitative biomarkers of oxidative/nitrosative stress, correlated to the progression of neurodegenerative lesions [50].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of Curcumin on Protein Damage Induced by Rotenone in Dopaminergic PC12 Cells

Buratta

Chiaradia

Tognoloni

et al. 2020

IJMS

View full text Add to dashboard Cite

Oxidative stress is considered to be a key factor of the pathogenesis of Parkinson’s disease, a multifactorial neurodegenerative disorder characterized by reduced dopaminergic neurons in the substantia nigra pars compacta and accumulated protein aggregates. Rotenone is a worldwide-used pesticide that induces the most common features of Parkinson’s by direct inhibition of the mitochondrial complex I. Rotenone-induced Parkinson’s models, as well as brain tissues from Parkinson’s patients, are characterized by the presence of both lipid peroxidation and protein oxidation markers resulting from the increased level of free radical species. Oxidation introduces several modifications in protein structure, including carbonylation and nitrotyrosine formation, which severely compromise cell function. Due to the link existing between oxidative stress and Parkinson’s disease, antioxidant molecules could represent possible therapeutic tools for this disease. In this study, we evaluated the effect of curcumin, a natural compound known for its antioxidant properties, in dopaminergic PC12 cells treated with rotenone, a cell model of Parkinsonism. Our results demonstrate that the treatment of PC12 cells with rotenone causes severe protein damage, with formation of both carbonylated and nitrotyrosine-derived proteins, whereas curcumin (10 µM) co-exposure exerts protective effects by reducing the levels of oxidized proteins. Curcumin also promotes proteasome activation, abolishing the inhibitory effect exerted by rotenone on this degradative system.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effect of Curcumin on Protein Damage Induced by Rotenone in Dopaminergic PC12 Cells

Buratta

Chiaradia

Tognoloni

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…Furthermore, another study confirmed that KLF6 exerted a promoting effect in macrophage inflammatory and hypoxic response (Kim et al, 2020 ). SOD, MDA, 3-NT, 8-OHdG, and GSH-Px are renowned oxidative stress indicators (Zhao et al, 2019 ; Bandookwala and Sengupta, 2020 ; Lv et al, 2020 ). Moreover, a prior study confirmed that the increased expression of SOD and GSH-Px and the diminished expression of MDA, 3-NT and 8-OHdG represented the alleviated oxidative stress (Liu et al, 2019 , 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Krüppel-Like Factor 6 Silencing Prevents Oxidative Stress and Neurological Dysfunction Following Intracerebral Hemorrhage via Sirtuin 5/Nrf2/HO-1 Axis

Sun

Cai

Chen

et al. 2021

Front. Aging Neurosci.

View full text Add to dashboard Cite

As a severe neurological deficit, intracerebral hemorrhage (ICH) is associated with overwhelming mortality. Subsequent oxidative stress and neurological dysfunction are likely to cause secondary brain injury. Therefore, this study sought to define the role of Krüppel-like factor 6 (KLF6) and underlying mechanism in oxidative stress and neurological dysfunction following ICH. An in vivo model of ICH was established in rats by injection of autologous blood, and an in vitro ICH cell model was developed in hippocampal neurons by oxyhemoglobin (OxyHb) exposure. Next, gain- and loss-of-function assays were performed in vivo and in vitro to clarify the effect of KLF6 on neurological dysfunction and oxidative stress in ICH rats and neuronal apoptosis and mitochondrial reactive oxygen species in OxyHb-induced hippocampal neurons. KLF6, nuclear factor erythroid 2–related factor 2 (Nrf2), and heme oxygenase 1 (HO-1) were highly expressed in hippocampal tissues of ICH rats, whereas sirtuin 5 (SIRT5) presented a poor expression. Mechanistically, KLF6 bound to the SIRT5 promoter and transcriptionally repressed SIRT5 to activate the Nrf2/HO-1 signaling pathway. KLF6 silencing alleviated neurological dysfunction and oxidative stress in ICH rats and diminished oxidative stress and neuronal apoptosis in OxyHb-induced neurons, whereas SIRT5 overexpression negated its effect. To sum up, KLF6 silencing elevated SIRT5 expression to inactivate the Nrf2/HO-1 signaling pathway, thus attenuating oxidative stress and neurological dysfunction after ICH.

show abstract

“…The release of NO and the generation of ONOO − induce a nitrosative stress that may alter folding, stability and activity of the target proteins [31]. While Dox increased the amount of nitrotyrosines in whole cell lysate from U-2OS cells but not from U-2OS/DX580 cells, NODox induced a robust and comparable nitration in both cell lines ( Fig.…”

Section: Nitric Oxide-releasing Doxorubicin Induces P-gp Nitration Fomentioning

confidence: 94%

Pleiotropic activities of nitric oxide-releasing doxorubicin on P-glycoprotein/ABCB1

2020

Journal of Molecular and Clinical Medicine

View full text Add to dashboard Cite

Doxorubicin is one of the first-line chemotherapeutic drugs for osteosarcoma, but the rate of success is below 60% of patients. The main cause of this low success is the presence of P-glycoprotein (P-gp/ABCB1) that effluxes the drug, limiting the intracellular accumulation and toxicity of Doxorubicin. P-gp also inhibits immunogenic cell death promoted by Doxorubicin. Nitric oxide-releasing Doxorubicin is a synthetic anthracycline effective against P-gppositive osteosarcoma cells. It is not known how it impacts on P-gp expression and immunogenic cell death induction. To address this point, we treated human Doxorubicinsensitive osteosarcoma U-2OS cells and their resistant variants with increasing amount of P-gp, with Dox and Nitric oxide-releasing Doxorubicin. While Doxorubicin was cytotoxic only in U-2OS cells, Nitric oxide-releasing Doxorubicin maintained its cytotoxic properties in all the resistant variants. Nitric oxide-releasing Doxorubicin elicited a strong nitrosative stress in whole cell extracts, endoplasmic reticulum and plasma membrane. P-gp was nitrated in all these compartments. The nitration caused protein ubiquitination and lower catalytic efficacy. The removal of P-gp from cell surface upon Nitric oxide-releasing Doxorubicin treatment disrupted its interaction with calreticulin, an immunogenic cell death-inducer that is inhibited by P-gp. Drug resistant cells treated with Nitric oxide-releasing Doxorubicin exposed calreticulin, were phagocytized by dendritic cells and expanded anti-tumor CD8 + T-lymphocytes. The efficacy of Nitric oxide-releasing Doxorubicin was validated in Dox-resistant osteosarcoma xenografts and was higher in immune-competent humanized mice than in immune-deficient mice, confirming that part of Nitric oxide-releasing Doxorubicin efficacy relies on the restoration of immunogenic cell death. Nitric oxide-releasing Doxorubicin was a pleiotropic anthracycline reducing activity and expression of P-gp, and restoring immunogenic cell death. It can be an innovative drug against P-gpexpressing/ Doxorubicin-resistant osteosarcomas.

show abstract

3-Nitrotyrosine: a versatile oxidative stress biomarker for major neurodegenerative diseases

Cited by 94 publications

References 131 publications

Effect of Curcumin on Protein Damage Induced by Rotenone in Dopaminergic PC12 Cells

Effect of Curcumin on Protein Damage Induced by Rotenone in Dopaminergic PC12 Cells

Krüppel-Like Factor 6 Silencing Prevents Oxidative Stress and Neurological Dysfunction Following Intracerebral Hemorrhage via Sirtuin 5/Nrf2/HO-1 Axis

Pleiotropic activities of nitric oxide-releasing doxorubicin on P-glycoprotein/ABCB1

Contact Info

Product

Resources

About