NAD in Skin

NAD in Skin

Abstract: The maintenance and regulation of cellular NAD(P)(H) content and its influence on cell function involves
many metabolic pathways, some of which remain poorly understood. Niacin deficiency in humans, which leads to low
NAD status, causes sun sensitivity in skin, indicative of deficiencies in responding to UV damage. Animal models of niacin
deficiency demonstrate genomic instability and increased cancer development in sensitive tissues including skin. Cell
culture models of niacin deficiency have allowed the identification of NAD-dependent signaling events critical in early
skin carcinogenesis. Niacin restriction in immortalized keratinocytes leads to an increased expression and activity of
NADPH oxidase resulting in an accumulation of ROS, providing a potential survival mechanism as has been shown to occur
in cancer cells. Niacin deficient keratinocytes are more sensitive to photodamage, as both poly(ADP-ribose) polymerases
and Sirtuins are inhibited by the unavailability of their substrate, NAD+, leading to unrepaired DNA damage upon
photodamage and a subsequent increase in cell death. Furthermore, the identification of the nicotinic acid receptor in human
skin keratinocytes provides a further link to niacin’s role as a potential skin cancer prevention agent and suggests the
nicotinic acid receptor as a potential target for skin cancer prevention agents. The new roles for niacin as a modulator of
differentiation and photo-immune suppression and niacin status as a critical resistance factor for UV damaged skin cells
are reviewed here.

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