NAD+ biosynthesis from tryptophan in the presence of nicotinic acid or vice versa by rat hepatocytes -: Effect of clofibrate-feeding

NAD(+) biosynthesis from tryptophan in the presence of nicotinic acid or vice versa by rat hepatocytes was investigated. In the control hepatocytes, NAD(+) synthesis from tryptophan was not affected by nicotinic acid from 0.026 to 0.26 mM. NAD(+) synthesis from nicotinic acid was slightly inhibited with varying concentration of tryptophan from 0.1 to 1.0 mM. In the clofibrate-treated hepatocytes, NAD(+) synthesis from tryptophan was greatly increased (234% of the control), while that from nicotinic acid was decreased (71.2% of the control). Both, NAD(+) synthesis from tryptophan and that from nicotinic acid were decreased by the coexisting nicotinic acid or tryptophan. Total amount of NAD(-) synthesized from tryptophan and nicotinic acid at their physiological concentrations was significantly higher than that in the control hepatocytes as a result of a large increase of NAD(-) synthesized from tryptophan. When the metabolic of 0.1 or 0.5 mM tryptophan was investigated, the glutarate pathway was suppressed in the clofibrate-treated hepatocytes, the quinolinic acid-NAD(+) flux being elevated. Similarly to clofibrate, DEHP and CPP revealed an increase in NAD(+) synthesis from tryptophan. Mutual relationship of NAD(+) biosyntheses from tryptophan and nicotinic acid in rat hepatocytes is discussed and the relevance with peroxisomal proliferation is suggested.