Abstract:
:We evaluated the autophagy-lysosomal pathway and membrane fluidity in brain cells and mitochondrial membranes obtained from senescence-accelerated (SAMP(8)) and senescence-resistant (SAMR(1)) 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 SAMP(8) compared to SAMR(1), 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 SAMP(8) than in SAMR(1) 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.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
García JJ,Piñol-Ripoll G,Martínez-Ballarín E,Fuentes-Broto L,Miana-Mena FJ,Venegas C,Caballero B,Escames G,Coto-Montes A,Acuña-Castroviejo Ddoi
10.1016/j.neurobiolaging.2009.12.013subject
Has Abstractpub_date
2011-11-01 00:00:00pages
2045-54issue
11eissn
0197-4580issn
1558-1497pii
S0197-4580(09)00406-0journal_volume
32pub_type
杂志文章abstract::Insomnia, daytime sleepiness, and nocturnal wandering, so common in the elderly, are caused largely by two specific pathophysiologic processes. Sleep apnea is a condition where respiration pauses during sleep, leading to arousal. Sleep apnea is due either to obstruction in the throat or failure of the central respirat...
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