Neurosci Lett. 2002 Nov 22;333(2):91-4.

The effects of nicotinamide on energy metabolism following transient focal cerebral ischemia in Wistar rats.

Yang J, Klaidman LK, Nalbandian A, Oliver J, Chang ML, Chan PH, Adams JD Jr.

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Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, 1985 Zonal Avenue, Los Angeles, CA 90089-9121, USA.

Abstract

This study examined the effects of nicotinamide on adenosine triphosphate (ATP) and nicotinamide adenine (NAD) levels and poly(adenosine diphosphate-ribose) (poly(ADP-ribose)) polymerase activity following ischemia and reperfusion in ketamine pretreated rats. Nicotinamide was administered at the end of the ischemic period. Nicotinamide protected against the depletion of ATP and NAD at 6 and 24 h of reperfusion. Nicotinamide is known to inhibit poly(ADP-ribose) polymerase at early time points, but was found to increase poly(ADP-ribose) polymerase activity at 24 h of reperfusion. It appears that nicotinamide can help maintain cellular energetics during reperfusion, thereby protecting cells from necrotic and apoptotic mechanisms.

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