Feeding Period of Selenium-Deficient Diet and Response of Redox Relating Minerals
Dynamics of redox relating biotrace elements, selenium (Se), iron (Fe), and zinc (Zn) in liver, kidney, and spleen of selenium deficient Wistar male rats in a series of feeding period (from 0 to 8 weeks) were studied using instrumental neutron activation analysis (INAA). Aspartate aminotransferase (...
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Veröffentlicht in: | Journal of Health Science 2006, Vol.52(6), pp.694-702 |
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creator | Matsumoto, Ken-ichiro Ariyoshi, Marie Terada, Sachiyo Okajo, Aya Urata, Hiromi Sakuma, Yasunobu Satoh, Kazue Ushio, Fusao Tsukada, Masamichi Endo, Kazutoyo |
description | Dynamics of redox relating biotrace elements, selenium (Se), iron (Fe), and zinc (Zn) in liver, kidney, and spleen of selenium deficient Wistar male rats in a series of feeding period (from 0 to 8 weeks) were studied using instrumental neutron activation analysis (INAA). Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and blood urea nitrogen (BUN) for the plasma fraction of the rat bloods and the concentration of vitamin C and vitamin E in the liver homogenates were measured. The initial purpose of this study was to find Fe and Zn as sensitive indices of the tissue oxidative stress levels. However, the relationships among the biotrace elements and the oxidative stress/injury were much complicated. Control group, which was fed Se-deficient diet with Na2SeO4 (0.1 mg selenium/l) in drinking water, showed strange response of Se and Zn contents in the kidney and showed high BUN. Supplementation of inorganic Se by biased Se source may serve as another source of a stress especially in the kidney. The Fe and Zn contents in the liver and kidney look sensitive to the Se-deficiency and/or relating oxidative stresses. Short term exposure to the Se-deficiency appeared to consume Fe and Zn in the liver and kidney. In contrast, long term or chronic exposure to Se-deficiency appeared to accumulate Fe and Zn in liver and kidney. |
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Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and blood urea nitrogen (BUN) for the plasma fraction of the rat bloods and the concentration of vitamin C and vitamin E in the liver homogenates were measured. The initial purpose of this study was to find Fe and Zn as sensitive indices of the tissue oxidative stress levels. However, the relationships among the biotrace elements and the oxidative stress/injury were much complicated. Control group, which was fed Se-deficient diet with Na2SeO4 (0.1 mg selenium/l) in drinking water, showed strange response of Se and Zn contents in the kidney and showed high BUN. Supplementation of inorganic Se by biased Se source may serve as another source of a stress especially in the kidney. The Fe and Zn contents in the liver and kidney look sensitive to the Se-deficiency and/or relating oxidative stresses. Short term exposure to the Se-deficiency appeared to consume Fe and Zn in the liver and kidney. 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Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and blood urea nitrogen (BUN) for the plasma fraction of the rat bloods and the concentration of vitamin C and vitamin E in the liver homogenates were measured. The initial purpose of this study was to find Fe and Zn as sensitive indices of the tissue oxidative stress levels. However, the relationships among the biotrace elements and the oxidative stress/injury were much complicated. Control group, which was fed Se-deficient diet with Na2SeO4 (0.1 mg selenium/l) in drinking water, showed strange response of Se and Zn contents in the kidney and showed high BUN. Supplementation of inorganic Se by biased Se source may serve as another source of a stress especially in the kidney. The Fe and Zn contents in the liver and kidney look sensitive to the Se-deficiency and/or relating oxidative stresses. Short term exposure to the Se-deficiency appeared to consume Fe and Zn in the liver and kidney. In contrast, long term or chronic exposure to Se-deficiency appeared to accumulate Fe and Zn in liver and kidney.</description><subject>bio-trace element</subject><subject>instrumental neutron activation analysis</subject><subject>mineral</subject><subject>oxidative stress</subject><subject>vitamin</subject><issn>1344-9702</issn><issn>1347-5207</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNpd0EFLwzAUB_AiCs7pxU9QEDwInUmaNO1JZHMqTNSp55Amr1tKl86kBf32ZlZ28PJeSH55PP5RdI7RBBOaX9drP2FkkhX0IBrhlPKEEcQPf880KTgix9GJ9zVCpEA5HkWvcwBt7Cp-AWdaHbdV_AYNWNNvkhlURhmwXTwz0MXS6ngJfttaDzu3BN1-hdrIbjfgyVhwsvGn0VEVGpz99XH0Mb97nz4ki-f7x-ntIlGMp11CMKM5ASBY6RKTnGFSFIjqjDHFUhruJFUZlUhqraqSFJxUOMcVK3EmeVml4-hymLt17WcPvhMb4xU0jbTQ9l7gIuOc5TTAi3-wbntnw24CU5rSAiOeB3U1KOVa7x1UYuvMRrpvgZHYZStCtoIREbIN-GbAte_kCvZUus6oBvZ0KOHH_kWtpRNg0x-81IJg</recordid><startdate>2006</startdate><enddate>2006</enddate><creator>Matsumoto, Ken-ichiro</creator><creator>Ariyoshi, Marie</creator><creator>Terada, Sachiyo</creator><creator>Okajo, Aya</creator><creator>Urata, Hiromi</creator><creator>Sakuma, Yasunobu</creator><creator>Satoh, Kazue</creator><creator>Ushio, Fusao</creator><creator>Tsukada, Masamichi</creator><creator>Endo, Kazutoyo</creator><general>The Pharmaceutical Society of Japan</general><general>Pharmaceutical Society of Japan, Nihon Yakugakkai</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>2006</creationdate><title>Feeding Period of Selenium-Deficient Diet and Response of Redox Relating Minerals</title><author>Matsumoto, Ken-ichiro ; Ariyoshi, Marie ; Terada, Sachiyo ; Okajo, Aya ; Urata, Hiromi ; Sakuma, Yasunobu ; Satoh, Kazue ; Ushio, Fusao ; Tsukada, Masamichi ; Endo, Kazutoyo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c573t-215482ee21cdb1285129904d655c534db1a4c64a0addcfb2972f181f5b16a7bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>bio-trace element</topic><topic>instrumental neutron activation analysis</topic><topic>mineral</topic><topic>oxidative stress</topic><topic>vitamin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsumoto, Ken-ichiro</creatorcontrib><creatorcontrib>Ariyoshi, Marie</creatorcontrib><creatorcontrib>Terada, Sachiyo</creatorcontrib><creatorcontrib>Okajo, Aya</creatorcontrib><creatorcontrib>Urata, Hiromi</creatorcontrib><creatorcontrib>Sakuma, Yasunobu</creatorcontrib><creatorcontrib>Satoh, Kazue</creatorcontrib><creatorcontrib>Ushio, Fusao</creatorcontrib><creatorcontrib>Tsukada, Masamichi</creatorcontrib><creatorcontrib>Endo, Kazutoyo</creatorcontrib><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Journal of Health Science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Matsumoto, Ken-ichiro</au><au>Ariyoshi, Marie</au><au>Terada, Sachiyo</au><au>Okajo, Aya</au><au>Urata, Hiromi</au><au>Sakuma, Yasunobu</au><au>Satoh, Kazue</au><au>Ushio, Fusao</au><au>Tsukada, Masamichi</au><au>Endo, Kazutoyo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Feeding Period of Selenium-Deficient Diet and Response of Redox Relating Minerals</atitle><jtitle>Journal of Health Science</jtitle><date>2006</date><risdate>2006</risdate><volume>52</volume><issue>6</issue><spage>694</spage><epage>702</epage><pages>694-702</pages><issn>1344-9702</issn><eissn>1347-5207</eissn><abstract>Dynamics of redox relating biotrace elements, selenium (Se), iron (Fe), and zinc (Zn) in liver, kidney, and spleen of selenium deficient Wistar male rats in a series of feeding period (from 0 to 8 weeks) were studied using instrumental neutron activation analysis (INAA). Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and blood urea nitrogen (BUN) for the plasma fraction of the rat bloods and the concentration of vitamin C and vitamin E in the liver homogenates were measured. The initial purpose of this study was to find Fe and Zn as sensitive indices of the tissue oxidative stress levels. However, the relationships among the biotrace elements and the oxidative stress/injury were much complicated. Control group, which was fed Se-deficient diet with Na2SeO4 (0.1 mg selenium/l) in drinking water, showed strange response of Se and Zn contents in the kidney and showed high BUN. Supplementation of inorganic Se by biased Se source may serve as another source of a stress especially in the kidney. The Fe and Zn contents in the liver and kidney look sensitive to the Se-deficiency and/or relating oxidative stresses. Short term exposure to the Se-deficiency appeared to consume Fe and Zn in the liver and kidney. In contrast, long term or chronic exposure to Se-deficiency appeared to accumulate Fe and Zn in liver and kidney.</abstract><cop>Tokyo</cop><pub>The Pharmaceutical Society of Japan</pub><doi>10.1248/jhs.52.694</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | bio-trace element instrumental neutron activation analysis mineral oxidative stress vitamin |
title | Feeding Period of Selenium-Deficient Diet and Response of Redox Relating Minerals |
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