Decreased Gene Expression of Testicular Cell-Specific Proteins in Cadmium-Induced Acute Testicular Toxicity

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著者

    • Nemoto Kiyomitsu Nemoto Kiyomitsu
    • Department of Molecular Toxicology and Global Center of Excellence (COE) Program, School of Pharmaceutical Sciences, University of Shizuoka
    • Miyajima Shoji Miyajima Shoji
    • Department of Molecular Toxicology and Global Center of Excellence (COE) Program, School of Pharmaceutical Sciences, University of Shizuoka
    • Hara Shiori [他] Hara Shiori
    • Department of Molecular Toxicology and Global Center of Excellence (COE) Program, School of Pharmaceutical Sciences, University of Shizuoka
    • Saigusa Ryosuke
    • Department of Molecular Toxicology and Global Center of Excellence (COE) Program, School of Pharmaceutical Sciences, University of Shizuoka
    • Yamada Masaki
    • Department of Molecular Toxicology and Global Center of Excellence (COE) Program, School of Pharmaceutical Sciences, University of Shizuoka
    • Sekimoto Masashi
    • Department of Molecular Toxicology and Global Center of Excellence (COE) Program, School of Pharmaceutical Sciences, University of Shizuoka
    • Degawa Masakuni
    • Department of Molecular Toxicology and Global Center of Excellence (COE) Program, School of Pharmaceutical Sciences, University of Shizuoka

抄録

Cadmium salts induce severe acute testicular necrosis in rodents. We assessed the expression levels of the genes encoding the follicle-stimulating hormone receptor, luteinizing hormone receptor, testis-specific histone 2B, and transition proteins 1 and 2, which are preferentially expressed in Sertoli cells, Leydig cells, spermatocytes, and spermatids, respectively, by reverse transcription (RT)-PCR using total RNA prepared from the whole testes of cadmium chloride (Cd)-administered rats. Spraque Dawley rats at 3, 7, and 12 weeks of age were singly and subcutaneously injected with Cd at doses of 1, 2.5, 5, 10, 15 or 20 μmol/kg. The expression levels of all genes tested were significantly decreased at doses of over 15 μmol/kg (3-week-old rats) or over 10 μmol/kg (7- and 12-week-old rats) 96 hr after injection. Histopathological study showed that these dosages of Cd resulted in extensive disruption of the seminiferous tubules and necrosis of testicular cells, while administration of Cd at a dose of 5 μmol/kg in 7- and 12-week-old rats resulted in only partial degeneration of seminiferous tubules and testicular cells. Therefore, their reduced gene expression is likely to serve as an indicator of Cd-induced testicular necrosis accompanied by cell death. In addition, the susceptibility to Cd-induced testicular damage and decreased gene expression was higher in mature (7- and 12-week-old) rats than in immature (3-week-old) rats.

収録刊行物

  • Journal of Health Science  

    Journal of Health Science 55(6), 952-956, 2009 

    The Pharmaceutical Society of Japan

各種コード

  • NII論文ID(NAID)
    130000127992
  • NII書誌ID(NCID)
    AA11316464
  • 本文言語コード
    EN
  • ISSN
    1344-9702
  • NDL 記事登録ID
    10456844
  • NDL 雑誌分類
    ZS17(科学技術--医学--衛生学・公衆衛生)
  • NDL 請求記号
    Z54-J464
  • データ提供元
    NDL  J-STAGE 
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