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Trophoblast toxicity of the neonicotinoid insecticide acetamiprid and an acetamiprid-based formulation.
Toxicology ( IF 4.5 ) Pub Date : 2020-01-11 , DOI: 10.1016/j.tox.2020.152363
Sebastian Diego Gomez 1 , Pamela Soledad Bustos 2 , Victoria Guadalupe Sánchez 3 , María Gabriela Ortega 4 , Natalia Guiñazú 1
Affiliation  

The neonicotinoid (Neo) insecticide family is a relatively new class of pesticides of growing use. There is an increasing concern that human exposure to environmental pollutants in utero may be associated with diseases in adulthood. A functional placenta and trophoblasts are a requisite for a healthy pregnancy. The aim of this study was to investigate whether the Neo Acetamiprid (Ace) and one of its commercial formulations (Ace CF) display toxic features to a human first trimester trophoblast cell line. HTR-8/SVneo cells were cultured in the presence of Ace or Ace CF (0.1-100 μM) for 4 and 24 h, and changes in cell viability, reactive oxygen species, antioxidant system and macromolecule damage levels were evaluated. Ace and Ace CF are cytotoxic for HTR-8/SVneo trophoblasts. Cell viability loss and oxidative imbalance were triggered by Ace and Ace CF treatments. Impact in the antioxidant enzymes catalase, superoxide dismutase and gluthatione S-transferase activities were observed after 24 h exposure to Ace CF. Moreover, Ace CF caused oxidative damage in proteins, lipids and DNA, whereas Ace only damaged proteins. To test oxidative stress as a toxicity mechanism, cells were pre-incubated with the antioxidant N-acetyl-l-cysteine (NAC), prior Neo treatment. NAC protected trophoblasts from cell death and prevented oxidative damage. Results demonstrate that Ace (as active principle or CF) is cytotoxic for human trophoblasts, and oxidative stress is a toxicity mechanism. Ace CF exhibited a more toxic effect than the active principle, in an identical exposure scenario.

中文翻译:

新烟碱类杀虫剂乙酰胺和基于乙酰胺的制剂的滋养细胞毒性。

新烟碱(Neo)杀虫剂家族是一类相对较新的农药,正在不断增加使用。人们越来越担心人类在子宫内暴露于环境污染物可能与成年期疾病有关。功能性胎盘和滋养细胞是健康怀孕的必要条件。这项研究的目的是调查新Ac虫(Ace)及其一种商业制剂(Ace CF)是否对人的早孕滋养层细胞系显示出毒性特征。将HTR-8 / SVneo细胞在Ace或Ace CF(0.1-100μM)存在下培养4和24小时,并评估细胞活力,活性氧种类,抗氧化剂系统和大分子损伤水平的变化。Ace和Ace CF对HTR-8 / SVneo滋养细胞具有细胞毒性。Ace和Ace CF处理可触发细胞活力丧失和氧化失衡。暴露于Ace CF 24小时后,观察到对抗氧化酶过氧化氢酶,超氧化物歧化酶和谷胱甘肽S-转移酶活性的影响。此外,Ace CF引起蛋白质,脂质和DNA的氧化损伤,而Ace仅损伤蛋白质。为了测试氧化应激作为一种毒性机制,在Neo治疗之前,将细胞与抗氧化剂N-乙酰基-1-半胱氨酸(NAC)预孵育。NAC保护滋养细胞免受细胞死亡,并防止氧化损伤。结果表明,Ace(作为活性成分或CF)对人类滋养细胞具有细胞毒性,氧化应激是一种毒性机制。在相同的暴露情况下,Ace CF比活性成分具有更强的毒性作用。暴露于Ace CF 24小时后,观察到超氧化物歧化酶和谷胱甘肽S-转移酶活性。此外,Ace CF引起蛋白质,脂质和DNA的氧化损伤,而Ace仅损伤蛋白质。为了测试氧化应激作为一种毒性机制,在Neo治疗之前,将细胞与抗氧化剂N-乙酰基-1-半胱氨酸(NAC)预孵育。NAC保护滋养细胞免受细胞死亡,并防止氧化损伤。结果表明,Ace(作为活性成分或CF)对人类滋养细胞具有细胞毒性,氧化应激是一种毒性机制。在相同的暴露情况下,Ace CF比活性成分具有更强的毒性作用。暴露于Ace CF 24小时后,观察到超氧化物歧化酶和谷胱甘肽S-转移酶活性。此外,Ace CF引起蛋白质,脂质和DNA的氧化损伤,而Ace仅损伤蛋白质。为了测试氧化应激作为一种毒性机制,在Neo治疗之前,将细胞与抗氧化剂N-乙酰基-1-半胱氨酸(NAC)预孵育。NAC保护滋养细胞免受细胞死亡,并防止氧化损伤。结果表明,Ace(作为活性成分或CF)对人类滋养细胞具有细胞毒性,氧化应激是一种毒性机制。在相同的暴露情况下,Ace CF比活性成分具有更强的毒性作用。而Ace只破坏蛋白质。为了测试氧化应激作为一种毒性机制,在Neo治疗之前,将细胞与抗氧化剂N-乙酰基-1-半胱氨酸(NAC)预孵育。NAC保护滋养细胞免受细胞死亡,并防止氧化损伤。结果表明,Ace(作为活性成分或CF)对人类滋养细胞具有细胞毒性,氧化应激是一种毒性机制。在相同的暴露情况下,Ace CF比活性成分具有更强的毒性作用。而Ace只破坏蛋白质。为了测试氧化应激作为一种毒性机制,在Neo治疗之前,将细胞与抗氧化剂N-乙酰基-1-半胱氨酸(NAC)预孵育。NAC保护滋养细胞免受细胞死亡,并防止氧化损伤。结果表明,Ace(作为活性成分或CF)对人类滋养细胞具有细胞毒性,氧化应激是一种毒性机制。在相同的暴露情况下,Ace CF比活性成分具有更强的毒性作用。氧化应激是一种毒性机制。在相同的暴露情况下,Ace CF比活性成分具有更强的毒性作用。氧化应激是一种毒性机制。在相同的暴露情况下,Ace CF比活性成分具有更强的毒性作用。
更新日期:2020-01-13
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