Nicotinamide as a precursor for NAD+ prevents apoptosis in the mouse brain induced by tertiary-butylhydroperoxide.
Neurosci Lett
; 206(1): 5-8, 1996 Mar 08.
Article
en En
| MEDLINE
| ID: mdl-8848280
The vitamin nicotinamide can protect against oxidative stress-induced apoptosis in the brain when used as a precursor for nicotinamide adenine dinucleotide (NAD+). The intracerebroventricular administration of tertiary-butylhydroperoxide (t-buOOH) to mice was used to simulate physiologic oxidative stress and apoptosis which may occur in some neurodegenerative conditions. t-buOOH produced characteristic apoptotic nuclear degeneration in neurons with extensive fragmentation of DNA. In this report we show that the elevation of NAD+ by nicotinamide prevents DNA fragmentation during apoptosis or necrosis in the brain as stimulated by t-buOOH administration. NAD+ levels can be increased by 50% in the brain. This may prevent the critical depletion of NAD+ by poly(ADP-ribose) polymerase (PARP) and provide additional substrate during the repair of DNA. Nicotinamide may be of particular interest in the treatment of neurodegeneration.
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Bases de datos:
MEDLINE
Asunto principal:
Peróxidos
/
Encéfalo
/
Apoptosis
/
Niacinamida
/
NAD
Límite:
Animals
Idioma:
En
Revista:
Neurosci Lett
Año:
1996
Tipo del documento:
Article
País de afiliación:
Estados Unidos