Person: López Torres, Mónica
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First Name
Mónica
Last Name
López Torres
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Ciencias Biológicas
Department
Genética, Fisiología y Microbiología
Area
Fisiología
Identifiers
7 results
Search Results
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Item Independent and additive effects of atenolol and methionine restriction on lowering rat heart mitochondria oxidative stress(Journal of Bioenergetics and Biomembranes, 2014) Sánchez-Román Rojas, Inés; Gómez, Alexia; Naudí, Alba; Jové, Mariona; Gómez, Jose; López Torres, Mónica; Pamplona, Reinald; Barja De Quiroga Losada, GustavoItem Adaptation to the European Space of Higher Education of the subject Projects and Studies in Biology(Edulearn 10. Conference Proceedings, 2010) Vacas, Ana María; Fonfría Díaz, José; Acosta Gallo, Belén; Alonso Gómez, Ángel Luis; Pedro Ormeño, Nuria de; Díez Sancho, Manuel; Fernández Pérez, Joaquín; López Torres, Mónica; Ramírez, Rosalía; Barrera, Alfonso; Reviriego, Mario; Gómez Chova, L.; Martí Belenguer, D.; Candel Torres, I.The subject projects and Studies in Biology is of a professional and applied nature, as the knowledge acquired can be applied in professional practice, because the students are initiated in the implementation of a Project (Planning, Alternative Solutions, Studies, Pre-projects and Projects. The general objective of this Project involved adapting the contents of the subject to the European Space of Higher Education (EEES) by installing it in the platform WebCT (Web Course Tools), adopted by Madrid's Complutense University for its Virtual Campus. The specific objectives to be met are the following: Conceptual objectives: To introduce students to the typology of Projects. This knowledge will enable people with a degree in Biology to work in Consultancy companies and different Organisms of the Administration and to adjust to the general work market. The students are also introduced to the Spanish System of Science and Technology and to the typology of Research Projects and Projects in collaboration with industries. Procedural objectives: handling procedures for searching for updated information, both offers and calls, and innovation in regulations or in science-technology and knowledge of software programs necessary for drafting a Budget for planning and implementing projects. Attitude-related projects: Considering that people with degrees in Biology traditionally work in Teaching and Research, this subject attempts to change the attitude of students towards what could involve practicing their profession in other areas tan these. In accordance wíth these objectives, the information on the development of the subject has been organized into a series of modules through which the basic knowledge the students should avail of is expounded. Each of these modules has línks to more elaborate documents in which the amount of material is increased and its implications and relationships with other contents of the subject are indicated. The modules are organízed into classes, practica! work aimed at problem- solving, common projects, presentation and debate, and the students must draft a Pre-project for implementation using the different documents it comprises. The subject requíres evaluation of the different conceptual, procedural and attitude-related objectives, and the general adoption of an ongoing evaluation process, in which the following aspects are evaluated: - Participation in classes requiring the presence of students, refresher courses and debates. - Evaluation of the seminars: presentation and defense of projects and of exercises completed. - Directed Academíc Work (creation and defense of a Pre-project with its corresponding documents). - Correct desígn of questionnaires. - Evaluation throughout the course with objective evaluation of the contents, by means of test-types exams.Item Effects of aging and methionine restriction applied at old age on ROS generation and oxidative damage in rat liver mitochondria(Biogerontology, 2012) Sánchez-Román Rojas, Inés; Gómez, Alexia; Pérez, Irene; Sánchez, Carlota; Suárez, Henar; Naudí, Alba; Jové, Mariona; López Torres, Mónica; Pamplona, Reinald; Barja De Quiroga Losada, GustavoIt is known that a global decrease in food ingestion (dietary restriction, DR) lowers mitochondrial ROS generation (mitROS) and oxidative stress in young immature rats. This seems to be caused by the decreased methionine ingestion of DR animals. This is interesting since isocaloric methionine restriction in the diet (MetR) also increases, like DR, rodent maximum longevity. However, it is not known if old rats maintain the capacity to lower mitROS generation and oxidative stress in response to MetR similarly to young immature animals, and whether MetR implemented at old age can reverse aging-related variations in oxidative stress. In this investigation the effects of aging and 7 weeks of MetR were investigated in liver mitochondria of Wistar rats. MetR implemented at old age decreased mitROS generation, percent free radical leak at the respiratory chain and mtDNA oxidative damage without changing oxygen consumption. Protein oxidation, lipoxidation and glycoxidation increased with age, and MetR in old rats partially or totally reversed these age-related increases. Aging increased the amount of SIRT1, and MetR decreased SIRT1 and TFAM and increased complex IV. No changes were observed in the protein amounts of PGC1, Nrf2, MnSOD, AIF, complexes I, II and III, and in the extent of genomic DNA methylation. In conclusion, treating old rats with isocaloric shortterm MetR lowers mitROS production and free radical leak and oxidative damage to mtDNA, and reverses aging-related increases in protein modification. Aged rats maintain the capacity to lower mitochondrial ROS generation and oxidative stress in response to a shortterm exposure to restriction of a single dietary substance: methionineItem Reduction in mitochondrialmembrane peroxidizability index and protein lipoxidation levels in therat heart after ß-adrenergic receptor signaling interruption with the ß-blocker atenolol(Anales de la Real Academia Nacional de Farmacia, 2013) Gomez, Alexia; Sánchez-Román Rojas, Inés; Gomez, Jose; Naudí, Alba; Pushparaj, Charumati; Portero-Otín, Manuel; López Torres, Mónica; Pamplona, Reinald; Barja De Quiroga Losada, GustavoItem Cysteine dietary supplementation reverses the decrease in mitochondrial ROS production at complex I induced by methionine restriction(Journal of Bioenergetics and Biomembranes, 2015) Gómez, A.; Gómez Sánchez, José; López Torres, Mónica; Naudí, Alba; Mota Martorrell, N.; Pamplona, R.; Barja de Quiroga, GustavoIt 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.Item 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(Aging Cell, 2014) Gómez, Alexia; Sánchez-Román Rojas, Inés; Gomez, Jose; Cruces, Julia; Mate, Ianire; López Torres, Mónica; Naudi, Alba; Portero-Otín, Manuel; Pamplona, Reinald; Fuente Del Rey, María Mónica De La; Barja De Quiroga Losada, GustavoThe 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.Item Rapamycin reverses age-related increases in mitochondrial ROS production at complex I, oxidative stress, accumulation of mtDNA fragments inside nuclear DNA, and lipofuscin level, and increases autophagy, in the liver of middle-aged mice(Experimental Gerontology, 2016) Martínez Cisuelo, V.; Gómez, J.; García Junceda, I.; Naudí, Alba; Cabré, R.; Mota Martorell, N.; López Torres, Mónica; González Sánchez, Mónica; Pamplona, R.; Barja de Quiroga, GustavoRapamycin consistently increases longevity in mice although the mechanism of action of this drug is unknown. In the present investigation we studied the effect of rapamycin on mitochondrial oxidative stress at the same dose that is known to increase longevity in mice (14 mg of rapamycin/kg of diet). Middle aged mice (16 months old) showed significant age-related increases in mitochondrial ROS production at complex I, accumulation of mtDNA fragments inside nuclear DNA, mitochondrial protein lipoxidation, and lipofuscin accumulation compared to young animals (4 months old) in the liver. After 7 weeks of dietary treatment all those increases were totally or partially (lipofuscin) abolished by rapamycin, middle aged rapamycin-treated animals showing similar levels in those parameters to young animals. The decrease in mitochondrial ROS production was due to qualitative instead of quantitative changes in complex I. The decrease in mitochondrial protein lipoxidation was not due to decreases in the amount of highly oxidizable unsaturated fatty acids. Rapamycin also decreased the amount of RAPTOR (of mTOR complex) and increased the amounts of the PGC1-α and ATG13 proteins. The results are consistent with the possibility that rapamycin increases longevity in mice at least in part by lowering mitochondrial ROS production and increasing autophagy, decreasing the derived final forms of damage accumulated with age which are responsible for increased longevity. The decrease in lipofuscin accumulation induced by rapamycin adds to previous information suggesting that the increase in longevity induced by this drug can be due to a decrease in the rate of aging.