Effects of heat stress on the redox status in the oviduct and early embryonic development in mice.
Effects of heat stress on the redox status in the oviduct and early embryonic development in mice.
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DOI：
10.1262/jrd.16089
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发表时间：
2005-02
期刊：
影响因子：
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通讯作者：
Takaya Matsuzuka;M. Ozawa;A. Nakamura;Atsuko Ushitani;M. Hirabayashi;Y. Kanai
中科院分区：
文献类型：
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作者：
Takaya Matsuzuka;M. Ozawa;A. Nakamura;Atsuko Ushitani;M. Hirabayashi;Y. Kanai
本研究探讨了热应激小鼠输卵管氧化还原状态与早期胚胎死亡之间的关系。在实验1中，未怀孕的小鼠在35℃、60%相对湿度下热应激12、24或36小时，通过测量输卵管中活性氧（ROS）水平和自由基清除活性（FRSA）水平，以及肝脏中硫代巴比妥酸活性物质（TBARS）和谷胱甘肽过氧化物酶（GSH-Px）活性来验证母体氧化还原状态。实验2，在妊娠当天热应激12 h的小鼠中收集受精卵，在体外评估其发育能力，以及2细胞期DNA损伤的强度。热应激小鼠肝脏中TBARS值和GSH-Px活性以及输卵管中ROS水平均显著升高，且这种升高似乎与热应激持续时间有关。母源热应激显著降低了桑葚胚和囊胚受精卵发育百分率和囊胚总细胞数。此外，母源热应激胚胎在2细胞期的DNA损伤显著较高。这些结果表明，热应激诱导母体氧化还原状态的系统性改变，由此导致的输卵管氧化应激的增加可能与热应激诱导的胚胎早期死亡有关。
This study examined the association between redox status in the oviduct and early embryonic death in heat-stressed mice. In Experiment 1, non-pregnant mice were heat-stressed at 35 C with 60% relative humidity for 12, 24, or 36 h, and the maternal redox status was verified by measuring the levels of reactive oxygen species (ROS) and free radical scavenging activity (FRSA) in the oviduct, and thiobarbituric acid reactive substances (TBARS) and glutathione peroxidase (GSH-Px) activity in the liver. In Experiment 2, zygotes were collected from mice heat-stressed for 12 h on the day of pregnancy, and their developmental abilities were assessed in vitro, along with the intensity of DNA damage at the 2-cell stage. The TBARS value and GSH-Px activity in the liver, and ROS level in the oviduct were significantly higher in heat-stressed mice, and this increase appeared to depend on the duration of the heat stress. Maternal heat stress significantly reduced the percentage of zygotes that developed to the morula and blastocyst and the total cell number in the blastocyst. In addition, DNA damage at the 2-cell stage was significantly higher in maternally heat-stressed embryos. These results suggest that heat stress induces systemic changes in redox status in the maternal body, and the resultant increase in oxidative stress in the oviduct is possibly involved in heat stress-induced early embryonic death .