Abstract:
: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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Klaidman LK,Mukherjee SK,Hutchin TP,Adams JDdoi
10.1016/0304-3940(96)12446-0subject
Has Abstractpub_date
1996-03-08 00:00:00pages
5-8issue
1eissn
0304-3940issn
1872-7972pii
0304394096124460journal_volume
206pub_type
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