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Dive into the research topics where Alexia Gomez is active.

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Featured researches published by Alexia Gomez.


Journal of Bioenergetics and Biomembranes | 2011

Methionine and homocysteine modulate the rate of ROS generation of isolated mitochondria in vitro

José Ignacio Gómez; Ines Sanchez-Roman; Alexia Gomez; Carlota Sanchez; Henar Suarez; Mónica López-Torres; Gustavo Barja

Dietary methionine restriction and supplementation in mammals have beneficial (antiaging) and detrimental effects respectively, which have been related to chronic modifications in the rate of mitochondrial ROS generation. However it is not known if methionine or its metabolites can have, in addition, direct effects on the rate of mitochondrial ROS production. This is studied here for the methionine cycle metabolites S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), homocysteine and methionine itself in isolated rat liver, kidney, heart, and brain mitochondria. The results show that methionine increases ROS production in liver and kidney mitochondria, homocysteine increases it in kidney and decreases it in the other three organs, and SAM and SAH have no effects. The variations in ROS production are localized at complexes I or III. These changes add to previously described chronic effects of methionine restriction and supplementation in vivo.


Journal of Bioenergetics and Biomembranes | 2015

Cysteine dietary supplementation reverses the decrease in mitochondrial ROS production at complex I induced by methionine restriction

Alexia Gomez; José Ignacio Gómez; M. López Torres; Alba Naudí; N. Mota-Martorell; Reinald Pamplona; Gustavo Barja

It has been described that dietary cysteine reverses many of the beneficial changes induced by methionine restriction in aging rodents. In this investigation male Wistar rats were subjected to diets low in methionine, supplemented with cysteine, or simultaneously low in methionine and supplemented with cysteine. The results obtained in liver showed that cysteine supplementation reverses the decrease in mitochondrial ROS generation induced by methionine restriction at complex I. Methionine restriction also decreased various markers of oxidative and non-oxidative stress on mitochondrial proteins which were not reversed by cysteine. Instead, cysteine supplementation also lowered protein damage in association with decreases in mTOR activation. The results of the present study add the decrease in mitochondrial ROS production to the various beneficial changes induced by methionine restriction that are reversed by cysteine dietary supplementation.


Aging Cell | 2014

Lifelong treatment with atenolol decreases membrane fatty acid unsaturation and oxidative stress in heart and skeletal muscle mitochondria and improves immunity and behavior, without changing mice longevity

Alexia Gomez; Ines Sanchez-Roman; José Ignacio Gómez; Julia Cruces; Ianire Maté; Mónica López-Torres; Alba Naudí; Manuel Portero-Otin; Reinald Pamplona; Mónica De la Fuente; Gustavo Barja

The membrane fatty acid unsaturation hypothesis of aging and longevity is experimentally tested for the first time in mammals. Lifelong treatment of mice with the β1‐blocker atenolol increased the amount of the extracellular‐signal‐regulated kinase signaling protein and successfully decreased one of the two traits appropriately correlating with animal longevity, the membrane fatty acid unsaturation degree of cardiac and skeletal muscle mitochondria, changing their lipid profile toward that present in much more longer‐lived mammals. This was mainly due to decreases in 22:6n‐3 and increases in 18:1n‐9 fatty acids. The atenolol treatment also lowered visceral adiposity (by 24%), decreased mitochondrial protein oxidative, glycoxidative, and lipoxidative damage in both organs, and lowered oxidative damage in heart mitochondrial DNA. Atenolol also improved various immune (chemotaxis and natural killer activities) and behavioral functions (equilibrium, motor coordination, and muscular vigor). It also totally or partially prevented the aging‐related detrimental changes observed in mitochondrial membrane unsaturation, protein oxidative modifications, and immune and behavioral functions, without changing longevity. The controls reached 3.93 years of age, a substantially higher maximum longevity than the best previously described for this strain (3.0 years). Side effects of the drug could have masked a likely lowering of the endogenous aging rate induced by the decrease in membrane fatty acid unsaturation. We conclude that it is atenolol that failed to increase longevity, and likely not the decrease in membrane unsaturation induced by the drug.


Journal of Bioenergetics and Biomembranes | 2014

Independent and additive effects of atenolol and methionine restriction on lowering rat heart mitochondria oxidative stress

Ines Sanchez-Roman; Alexia Gomez; Alba Naudí; Mariona Jové; José Ignacio Gómez; Mónica López-Torres; Reinald Pamplona; Gustavo Barja

A low rate of mitochondrial ROS production (mitROSp) and a low degree of fatty acid unsaturation are characteristic traits of long-lived animals and can be obtained in a single species by methionine restriction (MetR) or atenolol (AT) treatments. However, simultaneous application of both treatments has never been performed. In the present investigation it is shown that MetR lowers mitROSp and complex I content. Both the MetR and the AT treatments lower protein oxidative modification and oxidative damage to mtDNA and the fatty acid unsaturation degree in rat heart mitochondria. The decrease in fatty acid unsaturation seems to be due, at least in part, to decreases in desaturase and elongase activities or peroxisomal β-oxidation. Furthermore, the phosphorylation of extracellular signal-regulated kinase (ERK) was stimulated by MetR and AT. The decrease in membrane fatty acid unsaturation and protein oxidation, and the changes in fatty acids and p-ERK showed additive effects of both treatments. In addition, the increase in mitROSp induced by AT observed in the present investigation was totally avoided with the combined MetR + AT treatment. It is concluded that the simultaneous treatment with MetR plus atenolol is more beneficial than either single treatment alone to lower oxidative stress in rat heart mitochondria, analogously to what has been reported in long-lived animal species.


Journal of Bioenergetics and Biomembranes | 2011

Forty percent methionine restriction lowers DNA methylation, complex I ROS generation, and oxidative damage to mtDNA and mitochondrial proteins in rat heart

Ines Sanchez-Roman; Alexia Gomez; José Ignacio Gómez; Henar Suarez; Carlota Sanchez; Alba Naudí; Victoria Ayala; Manuel Portero-Otin; Mónica López-Torres; Reinald Pamplona; Gustavo Barja


Biogerontology | 2012

Effects of aging and methionine restriction applied at old age on ROS generation and oxidative damage in rat liver mitochondria

Ines Sanchez-Roman; Alexia Gomez; Irene Pérez; Carlota Sanchez; Henar Suarez; Alba Naudí; Mariona Jové; Mónica López-Torres; Reinald Pamplona; Gustavo Barja


Ophthalmology | 2007

Complement factor H.

M. de la Fuente; María José Blanco; Belen Pazos; M.I. Fernández; Angel Carracedo; Manuel Sánchez-Salorio; Rosa M. Coco; C. Torrón; Alexia Gomez


Biogerontology | 2016

Reduced apurinic/apyrimidinic endonuclease 1 activity and increased DNA damage in mitochondria are related to enhanced apoptosis and inflammation in the brain of senescence- accelerated P8 mice (SAMP8)

R. Torregrosa-Muñumer; Alexia Gomez; Elena Vara; Roman Kireev; Gustavo Barja; J. A. F. Tresguerres; Ricardo Gredilla


Anales De La Real Academia Nacional De Farmacia | 2013

La suplementación de larga duración con atenolol convierte la insaturación de las membranas mitocondriales de músculo esquelético y de corazón de ratón en la característica de mamíferos de supervivencia diez veces mayor. Efectos sobre la longevidad

Alexia Gomez; Alba Naudí; Reinaldo Pamplona; Gustavo Barja


Anales De La Real Academia Nacional De Farmacia | 2013

Long-life supplementation with atenolol converts the heart and skeletal muscle unsaturation of mitochondrial membranes of mice into those of ten fold longer-lived mammals. Effects on mean and maximum longevity

Alexia Gomez; Alba Naudí; Reinald Pamplona; Gustavo Barja de Quiroga

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Gustavo Barja

Complutense University of Madrid

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Ines Sanchez-Roman

Complutense University of Madrid

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Mónica López-Torres

Complutense University of Madrid

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José Ignacio Gómez

Complutense University of Madrid

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Carlota Sanchez

Complutense University of Madrid

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Henar Suarez

Complutense University of Madrid

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