Melatonin reduces membrane rigidity and oxidative damage in the brain of SAMP8 mice |
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Authors: | J.J. Garcí a,G. Piñ ol-RipollE. Martí nez-Ballarí n,L. Fuentes-BrotoF.J. Miana-Mena,C. VenegasB. Caballero,G. EscamesA. Coto-Montes,D. Acuñ a-Castroviejo |
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Affiliation: | a Department of Pharmacology and Physiology, University of Zaragoza, c) Domingo Miral s/n, 50009 Zaragoza, Spain b Department of Physiology, University of Granada, Avda. Madrid, 11, 18012 Granada, Spain c Department of Morphology and Cellular Biology, University of Oviedo, Avda. Julián Clavería 6, Oviedo, Spain |
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Abstract: | We evaluated the autophagy-lysosomal pathway and membrane fluidity in brain cells and mitochondrial membranes obtained from senescence-accelerated (SAMP8) and senescence-resistant (SAMR1) mice at 5 and 10 months of age. Moreover, we studied whether chronic treatment from age 1 to 10 months with melatonin stabilizes membrane fluidity. Fluidity was measured by polarization changes of 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene-p-toluene sulfonate. Results showed that in untreated animals at 5 months of age, synaptosomal and mitochondrial fluidity was decreased in SAMP8 compared to SAMR1, as was the cathepsin D/B ratio, indicating dysfunction of the autophagy-lysosomal pathway. Moreover, we detected synaptosomal rigidity and programmed cell death capability in both groups at 10 months of age. Mitochondrial fluidity, however, did not show a significant age-dependent change but was lower in SAMP8 than in SAMR1 at the 5- and 10-month time points. Melatonin administration prevented rigidity in the mitochondrial membrane and seemed to decrease age-related autophagy-lysosomal alterations. These data suggest that melatonin may act to slow down the aging process because of its ability to enhance membrane fluidity and maintain structural pathways. |
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Keywords: | Aging Melatonin Oxidative stress Membrane fluidity Mitochondria Senescence-accelerated mice |
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