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

Abstract：

: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 F(1)F(0)-ATP synthase is a molecular target of atrazine. A series of experiments with sperm and isolated mitochondria suggest that atrazine inhibits mitochondrial function through F(1)F(0)-ATP synthase. Moreover, affinity purification using atrazine as a ligand demonstrates that F(1)F(0)-ATP synthase is a major atrazine-binding protein in cells. The inhibitory activity against mitochondria and F(1)F(0)-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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Hase Y,Tatsuno M,Nishi T,Kataoka K,Kabe Y,Yamaguchi Y,Ozawa N,Natori M,Handa H,Watanabe H

doi

10.1016/j.bbrc.2007.11.107

subject

Has Abstract

pub_date

2008-02-01 00:00:00

pages

66-72

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(07)02493-X

journal_volume

366

pub_type

杂志文章

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