Browsing by Subject "Free radicals"

Now showing 1 - 6 of 6
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    Chronic administration of thiamine pyrophosphate decreases age-related histological atrophic testicular changes and improves sexual behavior in male Wistar rats
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Hernández-Montiel, H. L.; Vásquez López, C. M.; González-Loyola, J. G.; Vega-Anaya, G. C.; Villagrán-Herrera, M. E.; Gallegos-Corona, M. A.; Saldaña, C.; Ramos Gómez, M.; García Horshman, P.; García Solís, P.; Solís-S, J. C.; Robles-Osorio, M. L.; Ávila-Morales, J.; Varela-Echavarría, A.; Paredes Guerrero, R.
    Aging is a multifactorial universal process and constitutes the most important risk factor for chronic-degenerative diseases. Although it is a natural process, pathological aging arises when these changes occur quickly and the body is not able to adapt. This is often associated with the generation of reactive oxygen species (ROS), inflammation, and a decrease in the endogenous antioxidant systems, constituting a physiopathological state commonly found in chronicdegenerative diseases. At the testicular level, aging is associated with tissue atrophy, decreased steroidogenesis and spermatogenesis, and sexual behavior disorders. This situation, in addition to the elevated generation of ROS in the testicular steroidogenesis, provides a critical cellular environment causing oxidative damage at diverse cellular levels. To assess the effects of a reduction in the levels of ROS, thiamine pyrophosphate (TPP) was chronically administered in senile Wistar rats. TPP causes an activation of intermediate metabolism routes, enhancing cellular respiration and decreasing the generation of ROS. Our results show an overall decrease of atrophic histological changes linked to aging, with higher levels of serum testosterone, sexual activity, and an increase in the levels of endogenous antioxidant enzymes in TPP-treated animals. These results suggest that TPP chronic administration decreases the progression of age-related atrophic changes by improving the intermediate metabolism, and by increasing the levels of antioxidant enzymes.
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    Ferritin heavy chain as main mediator of preventive effect of metformin against mitochondrial damage induced by doxorubicin in cardiomyocytes
    (2014-02) Asensio Lopez, Maria del Carmen; Sanchez Mas, Jesus; Pascual Figal, Domingo A.; de la Torre, Carlos; Valdes, Mariano; Lax Pérez, Antonio Manuel; Medicina
    The efficacy of doxorubicin (DOX) as an antitumor agent is greatly limited by the induction of cardiomyopathy, which results from mitochondrial dysfunction and iron-catalyzed oxidative stress in the cardiomyocyte. Metformin (MET) has been seen to have a protective effect against the oxidative stress induced by DOX in cardiomyocytes through its modulation of ferritin heavy chain (FHC), the main iron-storage protein. This study aimed to assess the involvement of FHC as a pivotal molecule in the mitochondrial protection offered by MET against DOX cardiotoxicity. The addition of DOX to adult mouse cardiomyocytes (HL-1 cell line) increased the cytosolic and mitochondrial free iron pools in a time-dependent manner. Simultaneously, DOX inhibited complex I activity and ATP generation and induced the loss of mitochondrial membrane potential. The mitochondrial dysfunction induced by DOX was associated with the release of cytochrome c to the cytosol, the activation of caspase 3, and DNA fragmentation. The loss of iron homeostasis, mitochondrial dysfunction, and apoptosis induced by DOX were prevented by treatment with MET 24h before the addition of DOX. The involvement of FHC and NF-κB was determined through siRNA-mediated knockdown. Interestingly, the presilencing of FHC or NF-κB with specific siRNAs blocked the protective effect induced by MET against DOX cardiotoxicity. These findings were confirmed in isolated primary neonatal rat cardiomyocytes. In conclusion, these results deepen our knowledge of the protective action of MET against DOX-induced cardiotoxicity and suggest that therapeutic strategies based on FHC modulation could protect cardiomyocytes from the mitochondrial damage induced by DOX by restoring iron homeostasis
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    Is it coincidence that iron and melanin coexist in hepatic and other melanomacrophages?
    (Murcia : F. Hernández, 1990) Henninger, Jeanne M.; Beresford, W.A.
    Use of a Prussian-blue histochemical method shows iron in some but not all hepatic melanomacrophges of turtle, alligator, caiman and anole. The hypothesis prompted is that melanornacrophages in general synthesize melanin to render less noxious free radicals arising from catalysis by the iron.
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    Metformin protects against doxorubicin-induced cardiotoxicity: involvement of the adiponectin cardiac system
    (Elsevier, 2011-11-15) Asensio López, María del Carmen; Lax Pérez, Antonio Manuel; Pascual Figal, Domingo A; Valdés, Mariano; Sánchez Mas, Jesús; Medicina
    Doxorubicin has cardiotoxic effects that limit its clinical benefit in cancer patients. Metformin exerts cardioprotective actions via AMP-activated protein kinase (AMPK) and increases the expression of adiponectin and its receptors (adipoR1 and adipoR2) in skeletal muscle and adipose tissue, but its effect on cardiac tissue is still unknown. This work aimed to study whether metformin exerts any protective action against the cardiotoxicity of doxorubicin and whether the cardiac system of adiponectin is involved in any such action. The addition of doxorubicin (5μM) to adult mouse cardiomyocytes (HL-1 cell line) induced apoptosis, which was characterized by a loss of cell viability, activation of caspases, and fragmentation of the genetic material. Doxorubicin treatment also caused a decrease in the activity of the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase. Pretreatment with metformin (4mM, 24h) provided protection against doxorubicin-induced damage. This pretreatment significantly increased cell viability, attenuated the activation of caspases and the fragmentation of genetic material, and restored the antioxidant activity. In addition, metformin up-regulated the expression of adiponectin and its receptors, adipoR1 and adipoR2, in cardiomyocytes. In contrast, silencing either adipoR1 or adipoR2 with siRNA inhibited the AMPK activation and the protective effects of metformin. Taken together, these results demonstrate that metformin protects cardiomyocytes from doxorubicin-induced damage and that the cardiac adiponectin system plays an important role in this protective action.
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    On the importance of adequately choosing the ingredients of yoghurt and enriched milk for their antioxidant activity
    (Wiley, 2008-07-14) Jiménez Monreal, Antonia María; Murcia Tomás, María Antonia; Parras, Pilar; Martínez-Tomé, Magdalena; Tecnología de Alimentos, Nutrición y Bromatología
    The antioxidant activity of several dairy products, yoghurt enriched with green tea and lemon, fermented milk, yoghurt with strawberry pulp, ‘low-calorie’ yoghurt with inulin and milk enriched with vitamin E and their ingredients were analysed. Yoghurt enriched with green tea and lemon showed the best lipidic antioxidant capacity. All the dairy products analysed were very good OHÆ radical scavengers. The dairy products analysed were unable to scavenge H2O2 except green tea. The antioxidant activity of these samples resisted high temperatures in the Rancimat test; of the ingredients analysed, the best antioxidant activity was found for vitamin E followed by green tea, pectin, Lactobacillus acidophilus, lemon pulp and cornstarch. Antioxidant activity did not suffer variations during storage at an unfavourable temperature (40ºC), as demonstrated by the linoleic acid assay. Yoghurt enriched with green tea and lemon, yoghurt with strawberry pulp and low-calorie yoghurt with inulin produced the best results in the Trolox equivalent antioxidant capacity (TEAC) assay.
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    Vegetables antioxidant losses during industrial processing and refrigerated storage
    (Elsevier, 2009-10) Murcia, María Antonia; Jiménez Monreal, Antonia María; Martínez-Tomé, Magdalena; Tecnología de Alimentos, Nutrición y Bromatología
    Twenty-five vegetables (artichoke, asparagus, beetroot, broad bean, broccoli, Brussels sprout, carrot, cauliflower, celery, chicory, cucumber, eggplant, endive, garlic, green bean, leek, lettuce, maize, onion, pea, pepper, radish, spinach, Swiss chard and zucchini) were used to evaluate their antioxidant activity. All fresh vegetables studied were able to scavenge lipoperoxyl and hydroxyl radicals. All the vegetables also presented good total capacity antioxidant by TEAC assay except cucumber, endive, carrot and zucchini. Vegetables stored (7 days) in a home refrigerator recorded the same antioxidant activity as fresh samples, except cucumber and zucchini (lipid peroxidation) and broccoli, Brussels sprout and leek (TEAC). Canned vegetables showed a more pronounced loss of antioxidant activity than frozen vegetables compared with fresh vegetables. During the shelf life of the processed vegetables (8 months for frozen and 18 months for canned vegetables), some products showed losses (19–48%) of their lipoperoxyl radical scavenging capacity and total antioxidant activity