Association of status redox with demographic, clinical and imaging parameters in patients with Huntington's disease

Peña-Sánchez, Marisol; Riverón-Forment, Gretel; Zaldivar-Vaillant, Tatiana; Soto-Lavastida, Alexis; Borrero-Sánchez, Judith; Lara-Fernández, Gloria Esther; Esteban-Hernández, Enrique M.; Hernández-Díaz, Zenaida; González‐Quevedo, Alina; Fernández-Almirall, Isabel; Pérez-López, Claudia; Castillo-Casañas, Yaisa; Martínez-Bonne, Olivia; Cabrera-Rivero, Amelia; Valdés-Ramos, Leyenis; Guerra-Badía, Rosa; Fernández-Carriera, Rebeca; Menéndez-Sainz, María Caridad; González-García, Sergio

doi:10.1016/j.clinbiochem.2015.06.014

Cited by 22 publications

(19 citation statements)

References 35 publications

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“…PenaSanchez et al compared the activities of AOPP in 25 patients suffering from Alzheimer's disease and 30 healthy controls. They observed a significant difference in AOPP levels between control and patient groups (49). Recent investigations on the levels of AOPP in plasma and spinal liquid in amyotrophic sclerosis patients indicated the association of AOPP level with premature sclerosis and nervous tissue damages (50).…”

Section: Discussionmentioning

confidence: 99%

Serum Pro-Oxidant-Antioxidant Balance, Advanced Oxidized Protein Products (AOPP) and Protein Carbonyl in Patients With Stroke

Pouya¹,

Hashemy²,

Shoeibi³

et al. 2016

Razavi Int J Med

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Section: Discussionmentioning

confidence: 99%

Serum Pro-Oxidant-Antioxidant Balance, Advanced Oxidized Protein Products (AOPP) and Protein Carbonyl in Patients With Stroke

Pouya¹,

Hashemy²,

Shoeibi³

et al. 2016

Razavi Int J Med

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“…Huntington’s disease (HD) is a genetic, autosomal dominant disorder characterized by general neurodegeneration in brain with marked deterioration of medium-sized spiny neurons (MSNs) in the striatum [ 17 , 113 ]. HD is caused by a mutation (a CAG expansion) in the huntingtin gene ( HTT ), which results in an abnormal polyglutamine expansion in the huntingtin (HTT) protein and consequently HTT aggregation [ 113 ]. The mutant HTT alters intracellular Ca 2+ homeostasis, induces mitochondrial dysfunction, disrupts intracellular trafficking and impairs gene transcription [ 114 ].…”

Section: Role Of Vitamin C In Neurodegenerative Diseasesmentioning

confidence: 99%

Does Vitamin C Influence Neurodegenerative Diseases and Psychiatric Disorders?

et al. 2017

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Vitamin C (Vit C) is considered to be a vital antioxidant molecule in the brain. Intracellular Vit C helps maintain integrity and function of several processes in the central nervous system (CNS), including neuronal maturation and differentiation, myelin formation, synthesis of catecholamine, modulation of neurotransmission and antioxidant protection. The importance of Vit C for CNS function has been proven by the fact that targeted deletion of the sodium-vitamin C co-transporter in mice results in widespread cerebral hemorrhage and death on post-natal day one. Since neurological diseases are characterized by increased free radical generation and the highest concentrations of Vit C in the body are found in the brain and neuroendocrine tissues, it is suggested that Vit C may change the course of neurological diseases and display potential therapeutic roles. The aim of this review is to update the current state of knowledge of the role of vitamin C on neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, multiple sclerosis and amyotrophic sclerosis, as well as psychiatric disorders including depression, anxiety and schizophrenia. The particular attention is attributed to understanding of the mechanisms underlying possible therapeutic properties of ascorbic acid in the presented disorders.

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“…Oxidative damages in basal ganglia are found even in other degenerative disorders such multiple system atrophy, progressive supranuclear palsy and Huntington's disease [18][19][20]. Moreover, studies on biochemical changes occurring in Alzheimer's disease (AD), motor neuron disease and diabetic neuropathy also suggest the involvement of free radicals in neurodegeneration process [21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Effect of papaya supplementation on oxidative stress markers in Parkinsons disease

Bolner¹,

Micciolo²,

Bosello³

et al. 2016

Oxid Antioxid Med Sci

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Objective: In Parkinson's disease (PD), oxidative processes occur that are probably involved in the progression of neuronal damage. Recent studies suggest that regular consumption of antioxidant-rich foods or supplementation with functional foods like fermented papaya, may reduce cellular oxidative stress and protect against many agerelated diseases by strengthening the physiological antioxidant barrier. Our study aims to assess the antioxidant properties of a commercial fermented papaya preparation (FPP) in PD by evaluation of its effects on a wide panel of oxidative stress markers in blood and urine. Methods: A group of parkinsonian voluntary patients (T, n = 15) were treated 9 months with FPP and compared with a control group (NT, n = 12). The efficacy of FPP in increasing the physiological antioxidant barrier was evaluated at the times 0, 6 and 9 months with the analysis of 23 oxidative markers including total radical oxygen species, homocysteine, biological antioxidant potential, glutathione, superoxide dismutase, uric acid, total bilirubin, iron, ferritin, coenzyme Q10, 3-nitrotyrosine, total lipoperoxide, 4-hydroxy-nonenal, 8-hydroxydeoxyguanosine (8-OHdG) and 2-deoxyguanosine (2-dG). Results: Among the considered markers, twenty not showed significant differences at times 0, 6 and 9 months between T and NT patients, demonstrating a consequent non-significant effect of FPP supplementation. Instead, three urinary markers of oxidative stress on nucleic acids, 8-OHdG/2-dG, 2-dG/uric acid and 2-dG/creatinine showed statistical significant interactions between 'time' and 'treatment', highlighting an effective better response to oxidative attack for T than NT. Conclusions: Papaya supplementation for a medium-long time seems able to affect positively the turnover of oxidized nucleic acids helping to restore the normal nitrogenous bases into nucleotide chains and to replace those altered by radicals' attack.

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Association of status redox with demographic, clinical and imaging parameters in patients with Huntington's disease

Cited by 22 publications

References 35 publications

Serum Pro-Oxidant-Antioxidant Balance, Advanced Oxidized Protein Products (AOPP) and Protein Carbonyl in Patients With Stroke

Serum Pro-Oxidant-Antioxidant Balance, Advanced Oxidized Protein Products (AOPP) and Protein Carbonyl in Patients With Stroke

Does Vitamin C Influence Neurodegenerative Diseases and Psychiatric Disorders?

Effect of papaya supplementation on oxidative stress markers in Parkinsons disease

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