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Fosthiazate exposure induces oxidative stress, nerve damage, and reproductive disorders in nontarget nematodes
Environmental Science and Pollution Research Pub Date : 2022-09-16 , DOI: 10.1007/s11356-022-23010-y
Shiling Liu 1 , Qiqi Wu 1 , Yanru Zhong 1 , Zongzhe He 1 , Zhen Wang 1 , Rui Li 1 , Minghua Wang 1
Affiliation  

As a forceful nematicide, fosthiazate has been largely applied in the management of root-knot nematodes and other herbivorous nematodes. However, the toxicity of fosthiazate to nontarget nematodes is unclear. To explore the toxicity and the mechanisms of fosthiazate in nontarget nematodes, Caenorhabditis elegans was exposed to 0.01–10 mg/L fosthiazate. The results implied that treatment with fosthiazate at doses above 0.01 mg/L could cause injury to the growth, locomotion behavior, and reproduction of the nematodes. Moreover, L1 larvae were more vulnerable to fosthiazate exposure than L4 larvae. Reactive oxygen species (ROS) production and lipofuscin accumulation were fairly increased in 1 mg/L fosthiazate-exposed nematodes. Treatment with 0.1 mg/L fosthiazate significantly inhibited the activity of acetylcholinesterase (p < 0.01). Furthermore, subacute exposure to 10 mg/L fosthiazate strongly influenced the expression of genes related to oxidative stress, reproduction, and nerve function (e.g., gst-1, sod-1, puf-8, wee-1.3, and ace-1 genes). These findings suggested that oxidative stress, reproduction and nerve disorders could serve as key endpoints of toxicity induced by fosthiazate. The cyp-35a family gene was the main metabolic fosthiazate in C. elegans, and the cyp-35a5 subtype was the most sensitive, with a change in expression level of 2.11-fold compared with the control. These results indicate that oxidative stress and neurological and reproductive disorders played fundamental roles in the toxicity of fosthiazate in C. elegans and may affect the abundance and function of soil nematodes.

Graphical abstract



中文翻译:

噻唑磷暴露诱导非目标线虫的氧化应激、神经损伤和生殖障碍

作为一种强力杀线虫剂,噻唑磷已大量应用于根结线虫和其他食草线虫的防治。然而,噻唑磷对非目标线虫的毒性尚不清楚。探讨噻唑磷对非靶标线虫秀丽隐杆线虫的毒性及其作用机制暴露于 0.01–10 mg/L 噻唑磷。结果表明,使用剂量高于 0.01 mg/L 的噻唑磷处理可能会对线虫的生长、运动行为和繁殖造成伤害。此外,L1 幼虫比 L4 幼虫更容易受到磷噻唑的影响。在暴露于 1 mg/L 噻唑磷的线虫中,活性氧 (ROS) 的产生和脂褐素的积累显着增加。用 0.1 mg/L 噻唑磷处理显着抑制了乙酰胆碱酯酶的活性 ( p < 0.01)。此外,亚急性暴露于 10 mg/L 噻唑磷会强烈影响与氧化应激、生殖和神经功能相关的基因(例如gst-1sod-1puf-8wee-1.3 )的表达ace-1基因)。这些发现表明,氧化应激、生殖和神经障碍可以作为噻唑磷诱导的毒性的关键终点。cyp -35a家族基因是秀丽隐杆线虫主要代谢的噻唑磷,其中cyp-35a5亚型最为敏感,表达水平较对照变化2.11倍。这些结果表明,氧化应激以及神经和生殖障碍在硫唑磷对秀丽隐杆线虫的毒性中起着重要作用,并可能影响土壤线虫的数量和功能。

图形概要

更新日期:2022-09-17
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