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Feeding Period of Selenium-Deficient Diet and Response of Redox Relating Minerals

  • Matsumoto Ken-ichiro
    Department of Physical Chemistry, Showa Pharmaceutical University
  • Ariyoshi Marie
    Department of Physical Chemistry, Showa Pharmaceutical University
  • Terada Sachiyo
    Department of Physical Chemistry, Showa Pharmaceutical University
  • Okajo Aya
    Department of Physical Chemistry, Showa Pharmaceutical University
  • Urata Hiromi
    Department of Physical Chemistry, Showa Pharmaceutical University
  • Sakuma Yasunobu
    Department of Physical Chemistry, Showa Pharmaceutical University
  • Satoh Kazue
    Department of Anatomy, School of Medicine, Showa University
  • Ushio Fusao
    Office of Quality Assurance, Tokyo Metropolitan Institute of Public Health
  • Tsukada Masamichi
    Laboratory of Analytical Chemistry, School of Agriculture, Meiji University
  • Endo Kazutoyo
    Department of Physical Chemistry, Showa Pharmaceutical University

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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. <br>

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