Cadmium exposure increases susceptibility to testicular autoimmunity in mice

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  • Yuki Ogawa
    Department of Anatomy Tokyo Medical University Shinjuku 6‐1‐1 Shinjuku‐ku Tokyo 160‐8402 Japan
  • Masahiro Itoh
    Department of Anatomy Tokyo Medical University Shinjuku 6‐1‐1 Shinjuku‐ku Tokyo 160‐8402 Japan
  • Shuichi Hirai
    Department of Anatomy Tokyo Medical University Shinjuku 6‐1‐1 Shinjuku‐ku Tokyo 160‐8402 Japan
  • Shigeru Suna
    Department of Medical Technology Kagawa Prefectural University of Health Sciences Kagawa 761‐0123 Japan
  • Munekazu Naito
    Department of Anatomy Tokyo Medical University Shinjuku 6‐1‐1 Shinjuku‐ku Tokyo 160‐8402 Japan
  • Ning Qu
    Department of Anatomy Tokyo Medical University Shinjuku 6‐1‐1 Shinjuku‐ku Tokyo 160‐8402 Japan
  • Hayato Terayama
    Department of Anatomy Tokyo Medical University Shinjuku 6‐1‐1 Shinjuku‐ku Tokyo 160‐8402 Japan
  • Ayumi Ikeda
    Department of Anatomy Tokyo Medical University Shinjuku 6‐1‐1 Shinjuku‐ku Tokyo 160‐8402 Japan
  • Hidenobu Miyaso
    Department of Bioenvironmental Medicine, Graduate School of Medicine Chiba University Chuo‐ku Chiba 260‐8670 Japan
  • Yoshiharu Matsuno
    Department of Bioenvironmental Medicine, Graduate School of Medicine Chiba University Chuo‐ku Chiba 260‐8670 Japan
  • Masatoshi Komiyama
    Department of Bioenvironmental Medicine, Graduate School of Medicine Chiba University Chuo‐ku Chiba 260‐8670 Japan
  • Chisato Mori
    Department of Bioenvironmental Medicine, Graduate School of Medicine Chiba University Chuo‐ku Chiba 260‐8670 Japan

説明

<jats:title>ABSTRACT</jats:title><jats:p>Cadmium, one of various environmental toxicants, is known to suppress systemic immunity and to injure the testicular capillary endothelia with resultant necrosis of testicular tissues in mice and rats treated with high doses. Recently, it also became evident that cadmium can affect the integrity of the blood–testis barrier (BTB), the endocrine function of Leydig cells, apoptosis of germ cells and systemic immunity, even on treatment with a low dose that does not induce spermatogenic disturbance. Experimental autoimmune orchitis (EAO), i.e., an organ‐specific autoimmunity of the testis, can be induced by repeated immunization with testicular antigens, and its pathology is characterized by lymphocytic inflammation and spermatogenic disturbance. In the present study, we investigated the morphological and functional changes of testes in mice treated with a low dose of cadmium chloride (CdCl<jats:sub>2</jats:sub>) and also examined its toxicity as to susceptibility to EAO. The results showed that exposure to 3 mg CdCl<jats:sub>2</jats:sub> kg<jats:sup>−1</jats:sup> body weight did not affect the spermatogenic state. However, the BTB at the tubuli recti and the rete testis, but not the seminiferous tubules, was slightly weakened, and intra‐testicular mRNA expression of interleukin (IL)‐6, tumor necrosis factor‐<jats:italic>α</jats:italic> and IL‐1<jats:italic>β</jats:italic> was significantly increased by the CdCl<jats:sub>2</jats:sub> treatment. Furthermore, immunization with testicular antigens after the CdCl<jats:sub>2</jats:sub> exposure significantly augmented the EAO severity. Therefore, exposure to a low dose of CdCl<jats:sub>2</jats:sub> induces no significant disturbance of spermatogenesis, however, it does change the immunological microcircumstances in the testis, resulting in increased susceptibility to testicular autoimmunity. Copyright © 2012 John Wiley & Sons, Ltd.</jats:p>

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