Influence of adenine-induced renal failure on tryptophan-niacin metabolismin rats

To discover the role of the kidney in tryptophan degradation, especially tr yptophan to niacin, rat kidneys were injured by feeding a diet containing a large amount of adenine. The kidney contains very high activity of aminoca rboxymuconate-semialdehyde decarboxylase (ACMSD), which leads tryptophan in to the glutaric acid pathway and then the TCA cycle, but not to the niacin pathway. On the other hand, kidneys contain significant activity of quinoli nate phosphoribosyltransferase (QPRT), which leads tryptophan into the niac in pathway. The ACMSD activity in kidneys were significantly lower in the a denine group than in the control group, while the QPRT activity was almost the same, however, the formations of niacin and its compounds such as N-1-m ethylnicotinamide and its pyridones did not increase, and therefore, the co nversion ratio of tryptophan to niacin was lower in the adenine group than in the control group. The contents of NAD and NADP in liver, kidney, and bl ood were also lower in the adenine group. The decreased levels of niacin an d the related compounds were consistent with the changes in the enzyme acti vities involved in the tryptophan-niacin metabolism in liver. It was conclu ded from these results that the conversion of tryptophan to niacin is due t o only the liver enzymes and that the role of the kidney would be extremely low.