Literature DB >> 32719972

Oxidative stress biomarkers in Fabry disease: is there a room for them?

C Simoncini1, S Torri1, V Montano1, L Chico1, F Gruosso1, A Tuttolomondo2, A Pinto2, I Simonetta2, V Cianci3, A Salviati4, V Vicenzi5, G Marchi6, D Girelli6, D Concolino7, S Sestito7, M Zedde8, G Siciliano1, Michelangelo Mancuso9.   

Abstract

BACKGROUND: Fabry disease (FD) is an X-linked lysosomal storage disorder, caused by deficient activity of the alpha-galactosidase A enzyme leading to progressive and multisystemic accumulation of globotriaosylceramide. Recent data point toward oxidative stress signalling which could play an important role in both pathophysiology and disease progression.
METHODS: We have examined oxidative stress biomarkers [Advanced Oxidation Protein Products (AOPP), Ferric Reducing Antioxidant Power (FRAP), thiolic groups] in blood samples from 60 patients and 77 healthy controls.
RESULTS: AOPP levels were higher in patients than in controls (p < 0.00001) and patients presented decreased levels of antioxidant defences (FRAP and thiols) with respect to controls (p < 0.00001). In a small group of eight treatment-naïve subjects with FD-related mutations, we found altered levels of oxidative stress parameters and incipient signs of organ damage despite normal lyso-Gb3 levels.
CONCLUSIONS: Oxidative stress occurs in FD in both treated and naïve patients, highlighting the need of further research in oxidative stress-targeted therapies. Furthermore, we found that oxidative stress biomarkers may represent early markers of disease in treatment-naïve patients with a potential role in helping interpretation of FD-related mutations and time to treatment decision.

Entities:  

Keywords:  Biomarkers; Fabry disease; Oxidative stress; lysoGb3

Mesh:

Substances:

Year:  2020        PMID: 32719972      PMCID: PMC7674365          DOI: 10.1007/s00415-020-10044-w

Source DB:  PubMed          Journal:  J Neurol        ISSN: 0340-5354            Impact factor:   4.849


  31 in total

1.  Regional cerebral hyperperfusion and nitric oxide pathway dysregulation in Fabry disease: reversal by enzyme replacement therapy.

Authors:  D F Moore; L T Scott; M T Gladwin; G Altarescu; C Kaneski; K Suzuki; M Pease-Fye; R Ferri; R O Brady; P Herscovitch; R Schiffmann
Journal:  Circulation       Date:  2001-09-25       Impact factor: 29.690

2.  New mutations in the GLA gene in Brazilian families with Fabry disease.

Authors:  Lauro Thiago Turaça; Juliana Gilbert Pessoa; Fabiana Louise Motta; Maria Verônica Muñoz Rojas; Karen Barbosa Müller; Charles Marques Lourenço; Wilson Junior Marques; Vania D'Almeida; Ana Maria Martins; João Bosco Pesquero
Journal:  J Hum Genet       Date:  2012-05-03       Impact factor: 3.172

3.  The alpha-galactosidase A p.Arg118Cys variant does not cause a Fabry disease phenotype: data from individual patients and family studies.

Authors:  Susana Ferreira; Alberto Ortiz; Dominique P Germain; Miguel Viana-Baptista; António Caldeira-Gomes; Marta Camprecios; Maria Fenollar-Cortés; Ángel Gallegos-Villalobos; Diego Garcia; José Antonio García-Robles; Jesús Egido; Eduardo Gutiérrez-Rivas; José Antonio Herrero; Sebastián Mas; Raluca Oancea; Paloma Péres; Luis Manuel Salazar-Martín; Jesús Solera-Garcia; Helena Alves; Scott C Garman; João Paulo Oliveira
Journal:  Mol Genet Metab       Date:  2014-11-09       Impact factor: 4.797

4.  The ferric reducing ability of plasma (FRAP) as a measure of "antioxidant power": the FRAP assay.

Authors:  I F Benzie; J J Strain
Journal:  Anal Biochem       Date:  1996-07-15       Impact factor: 3.365

5.  Fabry disease: D313Y is an alpha-galactosidase A sequence variant that causes pseudodeficient activity in plasma.

Authors:  Roseline Froissart; Nathalie Guffon; Marie T Vanier; Robert J Desnick; Irene Maire
Journal:  Mol Genet Metab       Date:  2003-11       Impact factor: 4.797

6.  Advanced oxidation protein products as novel mediators of inflammation and monocyte activation in chronic renal failure.

Authors:  V Witko-Sarsat; M Friedlander; T Nguyen Khoa; C Capeillère-Blandin; A T Nguyen; S Canteloup; J M Dayer; P Jungers; T Drüeke; B Descamps-Latscha
Journal:  J Immunol       Date:  1998-09-01       Impact factor: 5.422

7.  Fabry disease: characterization of alpha-galactosidase A double mutations and the D313Y plasma enzyme pseudodeficiency allele.

Authors:  Makiko Yasuda; Junaid Shabbeer; Stacy D Benson; Irene Maire; Roger M Burnett; Robert J Desnick
Journal:  Hum Mutat       Date:  2003-12       Impact factor: 4.878

8.  Consensus recommendations for diagnosis, management and treatment of Fabry disease in paediatric patients.

Authors:  Dominique P Germain; Alain Fouilhoux; Stéphane Decramer; Marine Tardieu; Pascal Pillet; Marc Fila; Serge Rivera; Georges Deschênes; Didier Lacombe
Journal:  Clin Genet       Date:  2019-06-06       Impact factor: 4.438

9.  Evaluation of oxidative stress markers and cardiovascular risk factors in Fabry Disease patients.

Authors:  Karen B Müller; Luciano C Galdieri; Vanessa G Pereira; Ana M Martins; Vânia D'Almeida
Journal:  Genet Mol Biol       Date:  2012-05-17       Impact factor: 1.771

10.  Early initiation of enzyme replacement therapy in classical Fabry disease normalizes biomarkers in clinically asymptomatic pediatric patients.

Authors:  Amy Kritzer; Aishwarya Siddharth; Kate Leestma; Olaf Bodamer
Journal:  Mol Genet Metab Rep       Date:  2019-10-19
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  1 in total

1.  Inhibition of epigenetic reader proteins by apabetalone counters inflammation in activated innate immune cells from Fabry disease patients receiving enzyme replacement therapy.

Authors:  Li Fu; Sylwia Wasiak; Laura M Tsujikawa; Brooke D Rakai; Stephanie C Stotz; Norman C W Wong; Jan O Johansson; Michael Sweeney; Connie M Mohan; Aneal Khan; Ewelina Kulikowski
Journal:  Pharmacol Res Perspect       Date:  2022-06
  1 in total

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