María Luisa Ferrándiz
University of Valencia
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by María Luisa Ferrándiz.
Brain Research | 1994
María Luisa Ferrándiz; Marcos Martínez; Emilio de Juan; Araceli Díez; Gloria Bustos; Jaime Miquel
To elucidate the role of mitochondrial oxidative phosphorylation in neuronal aging, we have studied the activity of the respiratory complexes in the brain of young, adult and old mice. In synaptic mitochondria, we found a significant decrease in complexes IV (29%, P < 0.001) and V (21%, P < 0.01) in old as compared with adult mice. Nonsynaptic mitochondria also showed a senescent decrease in complexes I (15%, P < 0.01), II + III (34%, P < 0.01) and IV (17%, P < 0.01) activities. These findings suggest a dysfunction in mitochondrial oxidative phosphorylation in brain aging.
European Journal of Pharmacology: Environmental Toxicology and Pharmacology | 1995
Jaime Miquel; María Luisa Ferrándiz; Emilio de Juan; Immaculada Sevila; Marcos Martínez
Since it has been proposed that oxygen radical inactivation of key enzymes plays a critical role in cell aging, we have investigated the effects of a thiolic free radical scavenger on the oxidative phosphorylation enzymes of liver mitochondria from female OF-1 mice. At 48 weeks of age a control group was fed standard food pellets and another group received pellets containing 0.3% (w/w) of N-acetylcysteine. A 24-week treatment resulted in a significant increase in the specific activities of complex I, IV and V in the hepatic mitochondria of the N-acetylcysteine-treated animals as compared to aged controls.
British Journal of Pharmacology | 2004
María José Alcaraz; Ana María Vicente; Amparo Araico; José N. Domínguez; María Carmen Terencio; María Luisa Ferrándiz
The synthetic chalcone 3′,4′,5′,3,4,5‐hexamethoxy‐chalcone (CH) is an anti‐inflammatory compound able to reduce nitric oxide (NO) production by inhibition of inducible NO synthase protein synthesis. In this work, we have studied the mechanisms of action of this compound. CH (10–30 μM) prevents the overproduction of NO in RAW 264.7 macrophages stimulated with lipopolysaccharide (1 μg ml−1) due to the inhibition of nuclear factor κB (NF‐κB) activation. We have shown that treatment of cells with CH results in diminished degradation of the NF‐κB–IκB complex leading to inhibition of NF‐κB translocation into the nucleus, DNA binding and transcriptional activity. We also demonstrate the ability of this compound to activate NfE2‐related factor (Nrf2) and induce heme oxygenase‐1 (HO‐1). Our results indicate that CH determines a rapid but nontoxic increase of intracellular oxidative species, which could be responsible for Nrf2 activation and HO‐1 induction by this chalcone derivative. This novel anti‐inflammatory agent simultaneously induces a cytoprotective response (HO‐1) and downregulates an inflammatory pathway (NF‐κB) with a mechanism of action different from antioxidant chalcones.
Life Sciences | 1999
Marcos Martı́nez; Natividad Martı́nez; Ana Isabel Hernández; María Luisa Ferrándiz
Based on the finding of decreased mitochondrial complex I activity in the substantia nigra of patients with Parkinsons disease, we propose that the consequent reduction of ATP synthesis and increased generation of reactive oxygen species may be a possible cause of nigrostriatal cell death. Since sulfhydryl groups are essential in oxidative phosphorylation, thiolic antioxidants may contribute to the preservation of these proteins against oxidative damage. In the present paper, we hypothesize that treatment with a sulfur-containing antioxidant such as N-acetylcysteine may provide a new neuroprotective therapeutic strategy for Parkinsons disease.
Antioxidants & Redox Signaling | 2011
Nuria Maicas; María Luisa Ferrándiz; Rita Brines; Lidia Ibáñez; Antonio Cuadrado; Marije I. Koenders; Wim B. van den Berg; María José Alcaraz
AIMS Although oxidative stress participates in the etiopathogenesis of rheumatoid arthritis, its importance in this inflammatory disease has not been fully elucidated. In this study, we analyzed the relevance of the transcription factor Nrf2, master regulator of redox homeostasis, in the effector phase of an animal model of rheumatoid arthritis, using the transfer of serum from K/BxN transgenic mice to Nrf2(-/-) mice. RESULTS Nrf2 deficiency accelerated the incidence of arthritis, and animals showed a widespread disease affecting both front and hind paws. Therefore, the inflammatory response was enhanced, with increased migration of leukocytes and joint destruction in front paws. We observed an increased production of tumor necrosis factor-α, interleukin-6, and CXCL-1 in the joint, with small changes in eicosanoid levels. Serum levels of CXCL-1 and receptor activator for nuclear factor κB ligand were enhanced and osteocalcin decreased in arthritic Nrf2(-/-) mice. The expression of cyclooxygenase-2, inducible nitric oxide synthase, and peroxynitrite in the joints was higher in Nrf2 deficiency, whereas heme oxygenase-1 was downregulated. INNOVATION Nrf2 may be a therapeutic target for arthritis. CONCLUSION Our results support a protective role of Nrf2 against joint inflammation and degeneration in arthritis.
Brain Research | 1996
Marcos Jesús Iglesias Martínez; Ana Isabel Hernández; Natividad Martínez; María Luisa Ferrándiz
Since it has been proposed that oxidized protein accumulation plays a critical role in brain aging, we have investigated the effect of a thiolic antioxidant on protein carbonyl content in synaptic mitochondria from female OF-1 mice. At 48 weeks of age, a control group was fed standard food pellets and another group received pellets containing 0.3% (w/w) of N-acetylcysteine. A 24-week treatment resulted in a significant decrease in protein carbonyl content in synaptic mitochondria of the N-acetylcysteine-treated animals as compared to age-matched controls.
Brain Research | 1997
Marcos Martı́nez Banaclocha; Ana Isabel Hernández; Natividad Martı́nez; María Luisa Ferrándiz
Since it has been proposed that oxidized protein accumulation plays a critical role in brain aging, we have investigated their contents in synaptic mitochondria from five age groups of mice. Protein carbonyl content in synaptic mitochondria showed a significant positive correlation with age (r = 0.95, P = 0.01). A linear inverse relationship was observed between protein carbonyl content and complex IV/complex I ratio (which was used as an index of imbalance between mitochondrial respiratory complexes) in synaptic mitochondria in the five age groups (r = -0.99, P < 0.001). We suggest that age-related accumulation of oxidized proteins in synaptic mitochondria may be the result of an age-dependent increase in reactive oxygen species generation because of a disarrangement of mitochondrial oxidative phosphorylation.
Neuroscience Letters | 1994
Marcos Martńez; María Luisa Ferrándiz; Emilio de Juan; Jaime Miquel
To elucidate the contribution of lipid peroxides and glutathione to brain aging, we have carried out a comparative study of their contents in synaptic mitochondria from young (10-week-old), adult (24-week-old), and senescent (72-week-old) mice. In synaptic mitochondria, there is a significant decline in lipid peroxide content (P < 0.01) and cytochrome c oxidase activity (P < 0.001) in senescent as compared to adult and young mice. By contrast, glutathione concentration showed an increase in senescent (P < 0.05) in comparison to the other age groups. Moreover, there was a significant inverse correlation between age and lipid peroxide content (r = -0.5, P < 0.001) or cytochrome c oxidase-specific activity (r = -0.58, P < 0.001). We suggest that this age-dependent decrease in lipid peroxide content in synaptic mitochondria may be the result of an age-related decline in the activity of the electron transport chain, with concomitant decrease in oxyradical production, in the senescent organelles.
Journal of Pharmacy and Pharmacology | 1996
María Luisa Ferrándiz; Blanca Gil; Maria-Jesus Sanz; Amalia Ubeda; Silvia Erazo; Ernesto González; Rosa Negrete; Sergio Pacheco; Miguel Payáa; Maráa José Alcaraz
The effects of bakuchiol, a meroterpenoid isolated from the leaves of Psoralea glandulosa L., on phospholipase A2 (PLA2) activity from different sources, human neutrophil responses, zymosan air pouch and topical inflammation in mice, were investigated.
Journal of Nutritional Biochemistry | 2014
María Ángeles Rosillo; María José Alcaraz; Marina Sánchez-Hidalgo; José G. Fernández-Bolaños; Catalina Alarcón-de-la-Lastra; María Luisa Ferrándiz
The consumption of extra virgin olive oil (EVOO) in Mediterranean countries has shown beneficial effects. A wide range of evidence indicates that phenolic compounds present in EVOO are endowed with anti-inflammatory properties. In this work, we evaluated the effects of EVOO-polyphenol extract (PE) in a model of rheumatoid arthritis, the collagen-induced arthritis model in mice. On day 0, DBA-1/J mice were immunized with bovine type II collagen. On day 21, mice received a booster injection. PE (100 and 200 mg/kg) was orally administered once a day from days 29 to 41 to arthritic mice. We have demonstrated that PE decreases joint edema, cell migration, cartilage degradation and bone erosion. PE significantly reduced the levels of proinflammatory cytokines and prostaglandin E2 in the joint as well as the expression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1. Our data indicate that PE inhibits c-Jun N-terminal kinase, p38 and signal transducer and activator of transcription-3. In addition, PE decreases nuclear factor κB translocation leading to the down-regulation of the arthritic process. These results support the interest of natural diet components in the development of therapeutic products for arthritic conditions.