Reproductive Immunology and Biology
Online ISSN : 1881-7211
Print ISSN : 1881-607X
ISSN-L : 1881-607X
24 巻, 2 号
選択された号の論文の3件中1~3を表示しています
  • 伊藤 正裕
    2009 年 24 巻 2 号 p. 63-69
    発行日: 2009年
    公開日: 2011/06/16
    ジャーナル フリー
    Both reproduction and immunity are the roots to live for a creature. Evolutionally, the reproductive system developed earlier than the immune system. In particular, the appearance of lymphocytes was phylogenically delayed farther than that of sperm and ovum. Dr. Haeckel first documented that “ontogenesis is a brief and rapid recapitulation of phylogenesis”. However, lymphocytes mature ontogenically earlier than the appearance of haploid germ cells in a high creature. Therefore, the ontogenic relation between the reproductive and immune organs reverses with their phylogenic relation. Because the immune tolerance has already been established at puberty when the meiosis starts in gonads, the haploid but not the diploid cells express various autoimmunogenic antigens. This raises a possibility that self immune system attacks and rejects own haploid germ cells. In this review article, the author discuss a developmental contradiction of the relation between gonads and lymphoid organs in a high creature from both phylogenic and ontogenic aspects.
  • Kosuke Oikawa, Yoichi Matsuda, Masahiko Kuroda
    2009 年 24 巻 2 号 p. 70-76
    発行日: 2009年
    公開日: 2011/06/16
    ジャーナル フリー
    Environmental chemicals such as dioxin are known to have toxicities causing tumor promotion and serious reproductive and developmental defects. In this review, we focus on cell division, and discuss the effects of dioxin and related chemicals on the molecules involved in mitosis and/or meiosis. Dioxin affects various steps of biological processes including mitosis, meiosis, arrangement of chromosomal positioning and epigenetic regulation. Although the molecular mechanisms of these effects are still unclear, we provide recent findings of novel effects of dioxin and related compounds on them.
  • Koichi Nariai, Risa Fukumoto, Shin Onota, Ken Watanabe, Hiroshi Uchiya ...
    2009 年 24 巻 2 号 p. 77-80
    発行日: 2009年
    公開日: 2011/06/16
    ジャーナル フリー
    Excessive production of reactive oxygen species (ROS) lead to oxidative stress in tissue or organ dysfunction. To confirm ovarian dysfunction by ROS, ischemia-reperfusion (I/R) treatment of the ovarian blood vessels was performed using experimental rats in this study. Preventive effect of superoxide dismutase (SOD) as a radical scavenger against ovarian I/R injury was also examined. Hormonal sensitivities to equine chorionic gonadotropin (eCG) and human chorionic gonadotropin (hCG) in the ovary decreased after the I/R. Ovarian tissue and ovum destruction were also observed. These changes could be prevented by SOD administration. Our data suggest that I/R injury related to ROS production causes ovarian dysfunction. The dysfunction is prevented by administration of a radical scavenger.
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