Atrazine binds to F1F0-ATP synthase and inhibits mitochondrial function in sperm

Yasuyoshi Hase, Michiko Tatsuno, Takeyuki Nishi, Kosuke Kataoka, Yasuaki Kabe, Yuki Yamaguchi, Nobuaki Ozawa, Michiya Natori, Hiroshi Handa, Hajime Watanabe

Research output: Contribution to journalArticlepeer-review

47 Citations (Scopus)


Atrazine is a widely used triazine herbicide. Although controversy still exists, a number of recent studies have described its adverse effects on various animals including humans. Of particular interest is its effects on reproductive capacity. In this study, we investigated the mechanisms underlying the adverse effects of atrazine, with a focus on its effects on sperm. Here we show evidence that mitochondrial F1F0-ATP synthase is a molecular target of atrazine. A series of experiments with sperm and isolated mitochondria suggest that atrazine inhibits mitochondrial function through F1F0-ATP synthase. Moreover, affinity purification using atrazine as a ligand demonstrates that F1F0-ATP synthase is a major atrazine-binding protein in cells. The inhibitory activity against mitochondria and F1F0-ATP synthase is not limited to atrazine but is likely to be applicable to other triazine-based compounds. Thus, our findings may have wide relevance to pharmacology and toxicology.

Original languageEnglish
Pages (from-to)66-72
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - 2008 Feb 1
Externally publishedYes


  • Atrazine
  • FF-ATP synthase
  • Herbicide
  • Mitochondria
  • Sperm
  • Triazine

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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