Abstract
Nicotinamide is the primary precursor of nicotinamide adenine dinucleotide (NAD) [1], which is required for the manufacture of adenosine triphosphate (ATP) in the citric acid cycle (Fig. 11.1). Ultraviolet (UV) irradiation causes both DNA damage and depletion of cellular energy (NAD) [2], which is required for efficient DNA repair. Following UV irradiation, cellular NAD content is an important determinant of cell survival [2]. Human skin cells with reduced levels of NAD have a lower survival rate and higher genomic instability following UV exposure [2], whereas increased intracellular NAD is associated with enhanced protection against photo-oxidative stress [3]. As the precursor of NAD, nicotinamide would be expected to enhance DNA repair in UV-irradiated cells. At low concentrations (less than 3 mM), nicotinamide does enhance repair in UV-irradiated, repair-proficient cell lines, although with higher nicotinamide concentrations (5 mM), DNA repair returned to control levels [4].
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