首页> 美国卫生研究院文献>Oxidative Medicine and Cellular Longevity >Metallothionein-I/II Knockout Mice Aggravate Mitochondrial Superoxide Production and Peroxiredoxin 3 Expression in Thyroid after Excessive Iodide Exposure
【2h】

Metallothionein-I/II Knockout Mice Aggravate Mitochondrial Superoxide Production and Peroxiredoxin 3 Expression in Thyroid after Excessive Iodide Exposure

机译:金属硫蛋白-I / II敲除小鼠加重碘化物暴露后加重甲状腺线粒体超氧化物的产生和Peroxiredoxin 3的表达。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Purpose. We aim to figure out the effect of metallothioneins on iodide excess induced oxidative stress in the thyroid. Methods. Eight-week-old MT-I/II knockout (MT-I/II KO) mice and background-matched wild-type (WT) mice were used. Mitochondrial superoxide production and peroxiredoxin (Prx) 3 expression were measured. Results. In in vitro study, more significant increases in mitochondrial superoxide production and Prx 3 expression were detected in the MT-I/II KO groups. In in vivo study, significantly higher concentrations of urinary iodine level were detected in MT-I/II KO mice in 100 HI group. Compared to the NI group, there was no significant difference existing in serum thyroid hormones level in either groups (P > 0.05), while the mitochondrial superoxide production was significantly increased in 100 HI groups with significantly increased LDH activity and decreased relative cell viability. Compared to WT mice, more significant changes were detected in MT-I/II KO mice in 100 HI groups. No significant differences were detected between the NI group and 10 HI group in both the MT-I/II KO and WT mice groups (P > 0.05). Conclusions. Iodide excess in a thyroid without MT I/II protection may result in strong mitochondrial oxidative stress, which further leads to the damage of thyrocytes.
机译:目的。我们的目的是找出金属硫蛋白对碘过量诱导的甲状腺氧化应激的影响。方法。使用八周龄的MT-I / II基因敲除(MT-I / II KO)小鼠和背景匹配的野生型(WT)小鼠。测量线粒体超氧化物的产生和过氧化物酶(Prx)3的表达。结果。在体外研究中,在MT-I / II KO组中检测到线粒体超氧化物生成和Prx 3表达的更显着增加。在体内研究中,在100 HI组的MT-I / II KO小鼠中检测到明显更高的尿碘浓度。与NI组相比,两组中的血清甲状腺激素水平无显着差异(P> 0.05),而100个HI组中线粒体超氧化物的产生显着增加,LDH活性显着增加,相对细胞活力降低。与WT小鼠相比,在100个HI组的MT-I / II KO小鼠中检测到更显着的变化。在MT-I / II KO和WT小鼠组中,NI组和10 HI组之间均未检测到显着差异(P> 0.05)。结论。没有MT I / II保护的甲状腺中碘化物过量可能会导致强烈的线粒体氧化应激,进而导致甲状腺细胞受损。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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