男性不育的增加是全世界育龄夫妇面临的共同问题。已知二噁英(TCDD)，通过诱导氧化应激，引起精子发生异常, 是导致男性不育的重要因素。β-catenin 具有调节氧化应激的作用,但其在TCDD诱导的男性生殖系疾病中的作用机制尚不清楚。我们的前期工作发现，TCDD抑制β-catenin 的表达，且β-catenin 激动剂可降低TCDD 诱导的过氧化氢浓度，提示：TCDD 可能通过抑制β-catenin，降低抗氧化酶的表达，诱导氧化应激，导致精子发生异常。因此，我们将利用原代精原细胞和小鼠模型，研究TCDD 诱导的精子发生异常中β-catenin及其调节因子PI3K/AKT 的变化, 阐明β-catenin在TCDD 诱导的精子发生异常中对氧化应激的调节作用，揭示TCDD通过PI3K/AKT/β-catenin信号通路调控抗氧化酶的分子机制，为研究环境毒素所致的男性不育提供理论基础。

Increasing incidence of fertility is becoming the common issue of the world, and more and more infertile families suffer from it. Environmental pollutant, 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD), has been confirmed to affect spermatogenesis by inducing oxidative stress, apoptosis, and abnormal spermatogenesis. Recent studies have pointed out the regulating effects of β-catenin on oxidative stress, which could mediate cell proliferation, apoptosis. However, the roles of β-catenin in male infertility and mechanism for inducing oxidativce stress in TCDD-induced reproductive are not clear.The preliminary study has shown that β-catenin could be suppressed by TCDD treatment,and the β-catenin agonist could inhibit the increase of hydrogen peroxide produced by TCDD. Based on our and other team's the previous results, we hypothesize that TCDD could influence β-catenin and the related pathway to induce oxidative stress, and finally result in sperm abnormality. To clarify the roles of β-catenin in TCDD-induced toxicity ,we will observe the changes of β-catenin and the mediators, PI3K and AKT, find out the regulatory effects of β-catenin on TCDD-induced oxidative stress, and investigate the regulatory mechanisms of PI3K/AKT/β-catenin on antioxidants expression. We believe it could provide the theoretical basis for the environmental toxicants-induced diseases.