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首页> 外文期刊>Cellular Signalling >Thiamethoxam inhibits blastocyst expansion and hatching via reactive-oxygen species induced G2 checkpoint activation in pigs
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Thiamethoxam inhibits blastocyst expansion and hatching via reactive-oxygen species induced G2 checkpoint activation in pigs

机译：硫胺氧氧肟抑制胚泡膨胀和孵化通过反应性 - 氧物种诱导猪中的G2检查点激活

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Thiamethoxam (TMX) is a neonicotinoid insecticide. It has specific high toxicity to insects. Residues of TMX have been detected in various crops. Early embryo quality is vital for fertility. Excessive production of reactive oxygen species (ROS) can override embryonic antioxidant defenses, producing oxidative stress that triggers apoptosis, necrosis, and/or permanent DNA damage responses in the early embryo. Comparative studies have indicated that TMX hepatotoxicity is significant in mammals in acute tests, but little is known about accumulated chronic toxicity in early embryonic development. Porcine embryos were obtained here by the parthenogenetic activation of meiosis II oocytes and cultured in the PZM-5 medium with or without TMX. These embryos were evaluated by various methods. The expansion and hatching of blastocysts treated with TMX decreased by 21.73% and 16.71%, respectively, as compared with controls. In an analysis of 5-bromo-2-deoxyuridine (BrdU) incorporation, the rate of cell proliferation was 44.33% lower as compared with expanded blastocysts of the control group. ROS and gamma H2AX levels were higher in the TMX group than in the control group. Real-time reverse-transcription poly morose chain reaction showed that Sodl expression increased and the expression of Mnsod, Gpxl, Igta5, and Cox2 decreased. A CDK1 kinase assay revealed that maturation-promoting factor (MPF) activity diminished by 31.41% in expanding blastocysts. In conclusion, these results suggest that TMX inhibits blastocyst expansion and hatching by ROS-induced DNA damage checkpoint activation, which inhibits the activation of MPF and cell cycle progression in porcine blastocysts.
机译：硫胺（TMX）是一种新烟碱蛋白杀虫剂。它对昆虫具有特异性高毒性。在各种作物中检测到TMX的残留物。早期胚胎质量对生育是至关重要的。过度生产反应性氧（ROS）可以覆盖胚胎抗氧化防御，产生氧化应激，致胚，坏死和/或早期胚胎中的永久性DNA损伤反应。对比研究表明，TMX肝毒性在急性试验中哺乳动物显着，但在早期胚胎发育中累积的慢性毒性很少。这里通过过鼻肌II卵母细胞的单向激活并在具有或不具有TMX的PZM-5培养基中培养的猪胚胎。通过各种方法评估这些胚胎。与对照相比，用TMX处理的胚泡膨胀和阴压分别降低了21.73％和16.71％。在5-溴-2-脱氧尿苷（BRDU）掺入的分析中，与对照组的膨胀胚泡相​​比，细胞增殖的速率降低了44.33％。 TMX组ROS和γH2AX水平高于对照组。实时逆转录Poly More More Chain反应显示SODL表达增加和MNSOD，GPX1，IGTA5和COX2的表达降低。 CDK1激酶测定显示出现促进因子（MPF）活性在膨胀胚泡中减少了31.41％。总之，这些结果表明TMX通过ROS诱导的DNA损伤检查点激活抑制胚泡膨胀和孵化，这抑制了猪胚泡中MPF和细胞周期进展的激活。

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