Influence of adenine-induced renal failure on tryptophan-niacin metabolism in rats
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 in...
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| Veröffentlicht in: | Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2001-10, Vol.65 (10), p.2154-2161 |
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| creator | Fukuwatari, T. (Shiga Prefectural Univ., Hikone (Japan)) Morikawa, Y Hayakawa, F Sugimoto, E Shibata, K |
| description | 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. |
| doi_str_mv | 10.1271/bbb.65.2154 |
| format | Article |
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(Shiga Prefectural Univ., Hikone (Japan)) ; Morikawa, Y ; Hayakawa, F ; Sugimoto, E ; Shibata, K</creator><creatorcontrib>Fukuwatari, T. (Shiga Prefectural Univ., Hikone (Japan)) ; Morikawa, Y ; Hayakawa, F ; Sugimoto, E ; Shibata, K</creatorcontrib><description>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.</description><identifier>ISSN: 0916-8451</identifier><identifier>EISSN: 1347-6947</identifier><identifier>DOI: 10.1271/bbb.65.2154</identifier><identifier>PMID: 11758903</identifier><language>eng</language><publisher>Tokyo: Japan Society for Bioscience, Biotechnology, and Agrochemistry</publisher><subject>3-Hydroxyanthranilic Acid - metabolism ; ADENINE ; Adenine - administration & dosage ; ALDEHYDES ; aminocarboxymuconate-semialdehyde decarboxylase ; Animals ; Biological and medical sciences ; conversion ratio of tryptophan to niacin ; ENZYME ACTIVITY ; Kidney - enzymology ; KIDNEYS ; Kynurenic Acid - urine ; LIVER ; Liver - enzymology ; Male ; Medical sciences ; METABOLISM ; NAD - blood ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Niacin - metabolism ; Niacin - urine ; NICOTINAMIDE ; Quinolinic Acid - metabolism ; Quinolinic Acid - urine ; RATS ; Rats, Wistar ; renal deficiency ; Renal failure ; Renal Insufficiency - metabolism ; Renal Insufficiency - urine ; TRYPTOPHAN ; Tryptophan - metabolism ; Xanthurenates - urine</subject><ispartof>Bioscience, biotechnology, and biochemistry, 2001-10, Vol.65 (10), p.2154-2161</ispartof><rights>2001 by Japan Society for Bioscience, Biotechnology, and Agrochemistry 2001</rights><rights>2002 INIST-CNRS</rights><rights>Copyright Japan Science and Technology Agency 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c641t-b53a41f4cb91130c8c15c6d2dbdbb823fcd51b0adeef5900b8ae266e96ad4fac3</citedby><cites>FETCH-LOGICAL-c641t-b53a41f4cb91130c8c15c6d2dbdbb823fcd51b0adeef5900b8ae266e96ad4fac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13410294$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11758903$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fukuwatari, T. (Shiga Prefectural Univ., Hikone (Japan))</creatorcontrib><creatorcontrib>Morikawa, Y</creatorcontrib><creatorcontrib>Hayakawa, F</creatorcontrib><creatorcontrib>Sugimoto, E</creatorcontrib><creatorcontrib>Shibata, K</creatorcontrib><title>Influence of adenine-induced renal failure on tryptophan-niacin metabolism in rats</title><title>Bioscience, biotechnology, and biochemistry</title><addtitle>Biosci Biotechnol Biochem</addtitle><description>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.</description><subject>3-Hydroxyanthranilic Acid - metabolism</subject><subject>ADENINE</subject><subject>Adenine - administration & dosage</subject><subject>ALDEHYDES</subject><subject>aminocarboxymuconate-semialdehyde decarboxylase</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>conversion ratio of tryptophan to niacin</subject><subject>ENZYME ACTIVITY</subject><subject>Kidney - enzymology</subject><subject>KIDNEYS</subject><subject>Kynurenic Acid - urine</subject><subject>LIVER</subject><subject>Liver - enzymology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>METABOLISM</subject><subject>NAD - blood</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Niacin - metabolism</subject><subject>Niacin - urine</subject><subject>NICOTINAMIDE</subject><subject>Quinolinic Acid - metabolism</subject><subject>Quinolinic Acid - urine</subject><subject>RATS</subject><subject>Rats, Wistar</subject><subject>renal deficiency</subject><subject>Renal failure</subject><subject>Renal Insufficiency - metabolism</subject><subject>Renal Insufficiency - urine</subject><subject>TRYPTOPHAN</subject><subject>Tryptophan - metabolism</subject><subject>Xanthurenates - urine</subject><issn>0916-8451</issn><issn>1347-6947</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpt0NtrFDEUB-Agil2rTz4rA6IvZdZkcpnJoxQvlUKL6HM4uWlKJlmTGWT_e7PsSkEKgZDwncM5P4ReErwlw0jea623gm8HwtkjtCGUjb2QbHyMNlgS0U-MkzP0rNY7jNsHJ0_RGSEjnySmG_TtKvm4umRcl30H1qWQXB-SXY2zXXEJYuchxLU0kLql7HdL3v2C1KcAJqRudgvoHEOdu_YqsNTn6ImHWN2L032Ofnz6-P3yS3998_nq8sN1bwQjS685BUY8M1oSQrGZDOFG2MFqq_U0UG8sJxq3kZznEmM9gRuEcFKAZR4MPUfvjn13Jf9eXV3UHKpxMUJyea1qHCjF08gafPMfvMtraZtVRRiTjI4cj01dHJUpudbivNqVMEPZK4LVIWjVglaCq0PQTb8-9Vz17Oy9PSXbwNsTgGog-gLJhHrvKCN4kIdG4uhC8rnM8CeXaNUC-5jLvyL68ASvjoUesoKfpbmvtwPGhyOFoH8B6Eqhxw</recordid><startdate>20011001</startdate><enddate>20011001</enddate><creator>Fukuwatari, T. (Shiga Prefectural Univ., Hikone (Japan))</creator><creator>Morikawa, Y</creator><creator>Hayakawa, F</creator><creator>Sugimoto, E</creator><creator>Shibata, K</creator><general>Japan Society for Bioscience, Biotechnology, and Agrochemistry</general><general>Japan Society for Bioscience Biotechnology and Agrochemistry</general><general>Oxford University Press</general><scope>FBQ</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20011001</creationdate><title>Influence of adenine-induced renal failure on tryptophan-niacin metabolism in rats</title><author>Fukuwatari, T. (Shiga Prefectural Univ., Hikone (Japan)) ; Morikawa, Y ; Hayakawa, F ; Sugimoto, E ; Shibata, K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c641t-b53a41f4cb91130c8c15c6d2dbdbb823fcd51b0adeef5900b8ae266e96ad4fac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>3-Hydroxyanthranilic Acid - metabolism</topic><topic>ADENINE</topic><topic>Adenine - administration & dosage</topic><topic>ALDEHYDES</topic><topic>aminocarboxymuconate-semialdehyde decarboxylase</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>conversion ratio of tryptophan to niacin</topic><topic>ENZYME ACTIVITY</topic><topic>Kidney - enzymology</topic><topic>KIDNEYS</topic><topic>Kynurenic Acid - urine</topic><topic>LIVER</topic><topic>Liver - enzymology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>METABOLISM</topic><topic>NAD - blood</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Niacin - metabolism</topic><topic>Niacin - urine</topic><topic>NICOTINAMIDE</topic><topic>Quinolinic Acid - metabolism</topic><topic>Quinolinic Acid - urine</topic><topic>RATS</topic><topic>Rats, Wistar</topic><topic>renal deficiency</topic><topic>Renal failure</topic><topic>Renal Insufficiency - metabolism</topic><topic>Renal Insufficiency - urine</topic><topic>TRYPTOPHAN</topic><topic>Tryptophan - metabolism</topic><topic>Xanthurenates - urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fukuwatari, T. (Shiga Prefectural Univ., Hikone (Japan))</creatorcontrib><creatorcontrib>Morikawa, Y</creatorcontrib><creatorcontrib>Hayakawa, F</creatorcontrib><creatorcontrib>Sugimoto, E</creatorcontrib><creatorcontrib>Shibata, K</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Bioscience, biotechnology, and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fukuwatari, T. (Shiga Prefectural Univ., Hikone (Japan))</au><au>Morikawa, Y</au><au>Hayakawa, F</au><au>Sugimoto, E</au><au>Shibata, K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Influence of adenine-induced renal failure on tryptophan-niacin metabolism in rats</atitle><jtitle>Bioscience, biotechnology, and biochemistry</jtitle><addtitle>Biosci Biotechnol Biochem</addtitle><date>2001-10-01</date><risdate>2001</risdate><volume>65</volume><issue>10</issue><spage>2154</spage><epage>2161</epage><pages>2154-2161</pages><issn>0916-8451</issn><eissn>1347-6947</eissn><abstract>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.</abstract><cop>Tokyo</cop><pub>Japan Society for Bioscience, Biotechnology, and Agrochemistry</pub><pmid>11758903</pmid><doi>10.1271/bbb.65.2154</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Bioscience, biotechnology, and biochemistry, 2001-10, Vol.65 (10), p.2154-2161 |
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| source | J-STAGE Free; MEDLINE; Oxford University Press Journals All Titles (1996-Current); Freely Accessible Japanese Titles; EZB-FREE-00999 freely available EZB journals; Free Full-Text Journals in Chemistry |
| subjects | 3-Hydroxyanthranilic Acid - metabolism ADENINE Adenine - administration & dosage ALDEHYDES aminocarboxymuconate-semialdehyde decarboxylase Animals Biological and medical sciences conversion ratio of tryptophan to niacin ENZYME ACTIVITY Kidney - enzymology KIDNEYS Kynurenic Acid - urine LIVER Liver - enzymology Male Medical sciences METABOLISM NAD - blood Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Niacin - metabolism Niacin - urine NICOTINAMIDE Quinolinic Acid - metabolism Quinolinic Acid - urine RATS Rats, Wistar renal deficiency Renal failure Renal Insufficiency - metabolism Renal Insufficiency - urine TRYPTOPHAN Tryptophan - metabolism Xanthurenates - urine |
| title | Influence of adenine-induced renal failure on tryptophan-niacin metabolism in rats |
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