DIETARY NIACIN DEFICIENCY LOWERS TISSUE POLY(ADP-RIBOSE) AND NAD(-344RATS() CONCENTRATIONS IN FISCHER)

Poly(ADP-ribose) is synthesized in response to DNA strand breaks, usin g NAD(+) as substrate, and has been implicated in the process of DNA r epair. Because NAD(+) can be synthesized from niacin or tryptophan, bo th of these components must be manipulated to alter niacin status. Six dietary treatments were used, including niacin-deficient (ND) diets a nd niacin-replete (NR) diets consumed ad libitum and the NR diets pair -fed (PF) to the ND intake. The ND, NR and PF diets contained either 8 0 g casein + 50 g gelatin/kg diet (8-5 diets) or 70 g casein + 60 g ge latin/kg diet (7-6 diets) to control tryptophan content. The 8-5ND and 7-6ND diets induced mild and severe symptoms of niacin-deficiency, re spectively, over a 3-wk period in male weanling Fischer-344 rats. Food intake and weight gain were suppressed in both of the ND groups compa red with their- respective INR 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 P F 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 a nd 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 al so exerted an independent effect (PF levels were 46% of NR levels). Th ese data show that even a mild niacin deficiency decreases liver poly( ADP-ribose) concentrations and that poly(ADP-ribose) levels are altere d by food restriction in niacin-replete animals.