Mitochondria-related male infertility

作者：Nakada Kazuto^*; Sato Akitsugu; Yoshida Kayo; Morita Takashi; Tanaka Hiromitsu; Inoue Shin Ichi; Yonekawa Hiromichi; Hayashi Jun Ichi

来源：Proceedings of the National Academy of Sciences, 2006, 103(41): 15148-15153.

DOI：10.1073/pnas.0604641103

• meiosis
• mitochondrial diseases
• model mice
• respiration defects
• spermatogenesis

Approximately 15% of human couples are affected by infertility, and about half of these cases of infertility can be attributed to men, through low sperm motility (asthenozoospermia) or/and numbers (oligospermia). Because mitochondrial genome (mtDNA) mutations are identified in patients with fertility problems, there is a possibility that mitochondrial respiration defects contribute to male infertility. To address this possibility, we used a transmitochondrial mouse model (mito-mice) carrying wild-type mtDNA and mutant mtDNA with a pathogenic 4,696-bp deletion (Delta mtDNA). Here we show that mitochondrial respiration defects caused by the accumulation of Delta mtDNA induced oligospermia and asthenozoospermia in the mito-mice. Most sperm from the infertile mito-mice had abnormalities in the middle piece and nucleus. Testes of the infertile mito-mice showed meiotic arrest at the zygotene stage as well as enhanced apoptosis. Thus, our in vivo study using mito-mice directly demonstrates that normal mitochondrial respiration is required for mammalian spermatogenesis, and its defects resulting from accumulated mutant mtDNAs cause male infertility.

• 出版日期2006-10-10
• 单位河北医科大学