N-Acetylcysteine delays age-associated memory impairment in mice: role in synaptic mitochondria.
Mitochondrial oxidative damage is implicated in brain aging and in age-related neurodegenerative diseases. Since N-acetylcysteine (NAC) has recently been shown to prevent apoptotic death in neuronal cells and protect synaptic mitochondria proteins from oxidative damage in aged mice, we have investigated whether dietary administration of this thiolic antioxidant retards age-related memory loss. At 48 weeks of age, a control female OF-1 mice group was fed standard food pellets and another group received pellets containing 0.3% (w/w) of NAC. After 23 weeks of this diet, the NAC had partially restored the memory deficit associated with aging in mice. Moreover, the lipid peroxide and protein carbonyl contents of the synaptic mitochondria were significantly decreased in the NAC-supplemented animals in comparison with their age-matched controls. The antioxidant properties and probable action on mitochondrial bioenergetic ability in the synaptic terminals may explain, at least partially, the beneficial action of NAC administration.
Martínez
M
M
Department of Pathology, Hospital Universitario La Paz, Madrid, Spain.
Hernández
A I
AI
Martínez
N
N
D000111:Acetylcysteine / Q000494:pharmacology*; D000375:Aging / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects; D001522:Behavior, Animal / Q000187:drug effects; D005260:Female; D016166:Free Radical Scavengers / Q000494:pharmacology*; D008569:Memory Disorders / Q000188:drug therapy*; D051379:Mice; D008815:Mice, Inbred Strains; D008928:Mitochondria / Q000502:physiology*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D012044:Regression Analysis; D013569:Synapses / Q000502:physiology*
D016166:Free Radical Scavengers; D000111:Acetylcysteine