Melatonin reduces membrane rigidity and oxidative damage in the brain of SAMP8 mice

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 month...

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Published in:Neurobiology of aging 2011-11, Vol.32 (11), p.2045-2054
Main Authors: García, J.J, Piñol-Ripoll, G, Martínez-Ballarín, E, Fuentes-Broto, L, Miana-Mena, F.J, Venegas, C, Caballero, B, Escames, G, Coto-Montes, A, Acuña-Castroviejo, D
Format: Article
Language:English
Subjects:
Aging
Aging, Premature - metabolism
Animals
Brain - drug effects
Brain - metabolism
Cathepsin B - metabolism
Cathepsin D - metabolism
Cell Membrane - drug effects
Cell Membrane - metabolism
Female
Internal Medicine
Male
Melatonin
Melatonin - pharmacology
Membrane fluidity
Membrane Fluidity - drug effects
Mice
Mice, Transgenic
Mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Neurology
Oxidative stress
Oxidative Stress - drug effects
Senescence-accelerated mice
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Summary: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.
ISSN:0197-4580
1558-1497
DOI:10.1016/j.neurobiolaging.2009.12.013