Nicotinamide as a precursor for NAD+ prevents apoptosis in the mouse brain induced by tertiary-butylhydroperoxide.

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 Lett

journal_title

Neuroscience letters

authors

Klaidman LK,Mukherjee SK,Hutchin TP,Adams JD

doi

10.1016/0304-3940(96)12446-0

subject

Has Abstract

pub_date

1996-03-08 00:00:00

pages

5-8

issue

1

eissn

0304-3940

issn

1872-7972

pii

0304394096124460

journal_volume

206

pub_type

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