Dietary Niacin Deficiency Lowers Tissue Poly(ADP-Ribose) and NAD+ Concentrations in Fischer-344 Rats

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Abstract
Poly(ADP-ribose) is synthesized in response to DNA strand breaks, using NAD+ as substrate, and has been implicated in the process of DNA repair. Because NAD+ can be synthesized from niacin or tryptophan, both of these components must be manipulated to alter niacin status. Six dietary treatments were used, including niacin-deficient (ND) diets and niacin-replete (NR) diets consumed ad libitum and the NR diets pairfed (PF) to the ND intake. The ND, NR and PF diets contained either 80 g casein + 50 g gelatin/kg diet (8–5 diets) or 70 g casein + 60 g gelatin/kg diet (7–6 diets) to control tryptophan content. The 8-5ND and 7-6ND diets induced mild and severe symptoms of niacin deficiency, respectively, over a 3-wk period in male weanling Fischer-344 rats. Food intake and weight gain were suppressed in both of the ND groups compared with their respective NR controls. Weight gain was not different between ND animals and their PF counterparts. At 3 wk, blood, liver, kidney, heart and lung NAD+ concentrations for both 8-5ND and 7-6ND animals were all significantly lower than those for their respective PF groups. In the groups fed the 8-5 diets, liver poly(ADP-ribose) was lower in the ND group (64% of PF), with no difference between the NR and PF groups. In rats fed the 7-6 diets, poly(ADP-ribose) levels were further decreased in the ND group (43% of PF), but food restriction also exerted an independent effect (PF levels were 46% of NR levels). These data show that even a mild niacin deficiency decreases liver poly(ADP-ribose) concentrations and that poly(ADP-ribose) levels are altered by food restriction in niacin-replete animals.

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