Melatonin reduces membrane rigidity and oxidative damage in the brain of SAMP(8) mice

作者：Garcia J J^*; Pinol Ripoll G; Martinez Ballarin E; Fuentes Broto L; Miana Mena F J; Venegas C; Caballero B; Escames G; Coto Montes A; Acuna Castroviejo D

来源：Neurobiology of Aging, 2011, 32(11): 2045-2054.

DOI：10.1016/j.neurobiolaging.2009.12.013

• Aging
• Melatonin
• Oxidative stress
• Membrane fluidity
• Mitochondria
• Senescence-accelerated mice

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-trimethylammoniumpheny1)-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.

• 出版日期2011-11