...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research >Enhanced TGF-beta1 is involved in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced oxidative stress in C57BL/6 mouse testis.
【24h】

Enhanced TGF-beta1 is involved in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced oxidative stress in C57BL/6 mouse testis.

机译：增强的TGF-beta1参与C57BL / 6小鼠睾丸中的2,3,7,8-四氯二苯并-对-二恶英（TCDD）诱导的氧化应激。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

2,3,7,8-Tedtrachlorodibenzo-p-dioxin (TCDD) is one of the most toxic endocrine disruptors and has been reported to induce oxidative stress in the reproductive organs. However, the mechanism by which TCDD induces oxidative stress is unclear. The aim of this study is to examine the role of the general cytokine, TGF-beta1, in TCDD-induced oxidative stress in the male reproductive system. To examine the effect of TCDD on antioxidant enzyme activity, we administered TCDD orally to C57BL/6 mice at 1mug/kg/day for 4 days. Using Smad2-siRNA, we examined the involvement of Smad and non-Smad pathways in TCDD-induced oxidative stress. We also measured the mRNA levels of typical antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) and analyzed the activation of TGF-beta1, and the downstream signals, Smad2, Smad4, transcription factors (c-Jun, ATF3), and three major MAPKs (JNK, ERK, p38). After TCDD treatment, the mRNA levels of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) were significantly decreased. In addition, TGF-beta1 activity increased and the receptor-activated protein, Smad2, was activated while Smad4 was not. The levels of major transcription factors, c-Jun and ATF3, and the regulator of these transcription factors, MAPK, were also increased by TCDD administration. The mRNA levels of the 3 antioxidant enzymes in the Smad2-siRNA and TCDD co-treated group were higher than that of the TCDD-only treated group but still decreased when compared to control. C-Jun and ATF3 levels were also increased in Smad2-siRNA and TCDD co-treated testes compared to control. However, the levels of c-Jun and ATF3 were lower than those in the group treated with TCDD only. Of the three MAPKs which showed increase in expression after TCDD treatment, p38 was the only one that showed a decrease with Smad2 inhibition, while both ERK and JNK expression were unaffected. In conclusion, we found that the activated TGF-beta1-Smad pathway is involved in TCDD-induced oxidative stress. Furthermore, the effects of TCDD on the testes are caused by the coordinated action of both Smad and non-Smad pathways.
机译：2,3,7,8-四氯二苯并-对-二恶英（TCDD）是毒性最强的内分泌干扰物之一，据报道会在生殖器官中引起氧化应激。但是，TCDD诱导氧化应激的机制尚不清楚。这项研究的目的是检查男性生殖系统中一般细胞因子TGF-β1在TCDD诱导的氧化应激中的作用。为了检查TCDD对抗氧化酶活性的影响，我们以1mug / kg /天的剂量对C57BL / 6小鼠口服TCDD，共4天。使用Smad2-siRNA，我们检查了TCDD诱导的氧化应激中Smad和非Smad途径的参与。我们还测量了典型抗氧化酶（超氧化物歧化酶，过氧化氢酶，谷胱甘肽过氧化物酶）的mRNA水平，并分析了TGF-beta1，下游信号，Smad2，Smad4，转录因子（c-Jun，ATF3）和三种主要信号的活化MAPK（JNK，ERK，p38）。 TCDD处理后，抗氧化酶（超氧化物歧化酶，过氧化氢酶，谷胱甘肽过氧化物酶）的mRNA水平显着降低。此外，TGF-beta1活性增加，受体激活蛋白Smad2被激活，而Smad4没有。 TCDD给药也增加了主要转录因子c-Jun和ATF3的水平，以及这些转录因子MAPK的调节剂。 Smad2-siRNA和TCDD共治疗组中3种抗氧化酶的mRNA水平高于仅TCDD治疗组，但与对照组相比仍下降。与对照相比，Smad2-siRNA和TCDD共同治疗的睾丸中C-Jun和ATF3水平也增加。然而，c-Jun和ATF3的水平低于仅用TCDD治疗的组。在TCDD处理后三个表达增加的MAPK中，p38是唯一一个被Smad2抑制降低的MAPK，而ERK和JNK的表达均不受影响。总之，我们发现激活的TGF-β1-Smad途径与TCDD诱导的氧化应激有关。此外，TCDD对睾丸的影响是由Smad和非Smad途径的协同作用引起的。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号