Influence of adenine-induced renal failure on tryptophan-niacin metabolism in rats

被引:27
作者
Fukuwatari, T [1 ]
Morikawa, Y [1 ]
Hayakawa, F [1 ]
Sugimoto, E [1 ]
Shibata, K [1 ]
机构
[1] Univ Shiga Prefecture, Course Food Sci & Nutr, Dept Life Style Studies, Sch Human Cultures, Shiga 5228533, Japan
关键词
renal deficiency; tryptophan metabolism; nicotinamide; conversion ratio of tryptophan to niacin; aminocarboxymuconate-semialdehyde; decarboxylase;
D O I
10.1271/bbb.65.2154
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
To discover the role of the kidney in tryptophan degradation, especially tryptophan to niacin, rat kidneys were injured by feeding a diet containing a large amount of adenine. The kidney contains very high activity of aminocarboxymuconate-semialdehyde decarboxylase (ACMSD), which leads tryptophan into the glutaric acid pathway and then the TCA cycle, but not to the niacin pathway. On the other hand, kidneys contain significant activity of quinolinate phosphoribosyltransferase (QPRT), which leads tryptophan into the niacin pathway. The ACMSD activity in kidneys were significantly lower in the adenine 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-methylnicotinamide and its pyridones did not increase, and therefore, the conversion 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 blood were also lower in the adenine group. The decreased levels of niacin and the related compounds were consistent with the changes in the enzyme activities involved in the tryptophan-niacin metabolism in liver. It was concluded from these results that the conversion of tryptophan to niacin is due to only the liver enzymes and that the role of the kidney would be extremely low.
引用
收藏
页码:2154 / 2161
页数:8
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