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Niacin requirements for genomic stability

Authors :
Kirkland, James B.
Source :
Mutation Research: Fundamental & Molecular Mechanisms of Mutagenesis. May2012, Vol. 733 Issue 1/2, p14-20. 7p.
Publication Year :
2012

Abstract

Abstract: Through its involvement in over 400 NAD(P)-dependent reactions, niacin status has the potential to influence every area of metabolism. Niacin deficiency has been linked to genomic instability largely through impaired function of the poly ADP-ribose polymerase (PARP) family of enzymes. In various models, niacin deficiency has been found to cause impaired cell cycle arrest and apoptosis, delayed DNA excision repair, accumulation of single and double strand breaks, chromosomal breakage, telomere erosion and cancer development. Rat models suggest that most aspects of genomic instability are minimized by the recommended levels of niacin found in AIN-93 formulations; however, some beneficial responses do occur in the range from adequate up to pharmacological niacin intakes. Mouse models show a wide range of protection against UV-induced skin cancer well into pharmacological levels of niacin intake. It is currently a challenge to compare animal and human data to estimate the role of niacin status in the risk of genomic instability in human populations. It seems fairly certain that some portion of even affluent populations will benefit from niacin supplementation, and some subpopulations are likely well below an optimal intake of this vitamin. With exposure to stressors, like chemotherapy or excess sunlight, suraphysiological doses of niacin may be beneficial. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
00275107
Volume :
733
Issue :
1/2
Database :
Academic Search Index
Journal :
Mutation Research: Fundamental & Molecular Mechanisms of Mutagenesis
Publication Type :
Academic Journal
Accession number :
75010184
Full Text :
https://doi.org/10.1016/j.mrfmmm.2011.11.008