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.