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

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 mela...

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Veröffentlicht in:Neurobiology of aging Jg. 32; H. 11; S. 2045 - 2054
Hauptverfasser: 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: Journal Article
Sprache:Englisch
Veröffentlicht: United States Elsevier Inc 01.11.2011
Schlagworte:
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
Aging
Oxidative stress
Senescence-accelerated mice
Melatonin
Membrane fluidity
Mitochondria
ISSN:0197-4580, 1558-1497, 1558-1497
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Zusammenfassung: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.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0197-4580
1558-1497
1558-1497
DOI:10.1016/j.neurobiolaging.2009.12.013