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
5 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 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 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.