Chemosphere ( IF 8.1 ) Pub Date : 2021-03-01 , DOI: 10.1016/j.chemosphere.2021.130120 Stephanie A. Maggio , Philip K. Janney , Jeffrey J. Jenkins
Chlorpyrifos (CPF) is a widely used broad-spectrum organophosphate insecticide. CPF elicits neurotoxic effects in exposed organisms by inhibiting the activity of acetylcholinesterase enzymes (AChE), which prolongs nerve transmission and results in neurotoxic symptoms and death at high doses. While CPF is capable of eliciting neurotoxic effects, chlorpyrifos-oxon (CPFO) is the primary neurotoxicant agent. Aquatic organisms bioactivate CPF to CPFO through the Cytochrome P450 phase I metabolic pathway following exposure to CPF. Additionally, in the environment, CPF transforms to CPFO, primarily through photo-oxidation. As both compounds can be transported in air and water to aquatic ecosystems, there is the potential for exposure to non-target organisms. The potential for adverse impacts on aquatic receptors depends on patterns of exposure and toxicity of individual compounds and the mixture. To study the neurotoxicity of these compounds, a 48-hour acute and 21-day chronic Daphnia magna bioassay were conducted independently with CPF and CPFO. Acute bioassay results show a median lethal concentration (LC50) of 0.76 μg/L for CPF and 0.32 μg/L for CPFO, suggesting that CPFO is 2.4 times more acutely toxic to D. magna. Acute assay results were also used to derive Benchmark Dose Levels of 0.58 μg/L for CPF and 0.25 μg/L for CPFO. However, neither compound elicited an effect on reproduction or growth at relevant chronic exposures. As D. magna are a small and therefore a relatively sensitive species, and the AChE inhibition adverse outcome pathway is highly conserved, these results may be cautiously extrapolated in assessing adverse impacts on aquatic receptors.1
中文翻译:
毒死rif和毒死rif对大蚤的神经毒性
毒死rif(CPF)是一种广泛使用的广谱有机磷杀虫剂。CPF通过抑制乙酰胆碱酯酶(AChE)的活性在暴露的生物体中引起神经毒性作用,这会延长神经传递并导致高剂量的神经毒性症状和死亡。虽然CPF能够引起神经毒性作用,但毒死rif-氧氟沙星(CPFO)是主要的神经毒性剂。暴露于CPF后,水生生物通过细胞色素P450 I期代谢途径将CPF生物活化为CPFO。此外,在环境中,CPF主要通过光氧化转化为CPFO。由于两种化合物都可以在空气和水中运输到水生生态系统,因此有可能暴露于非目标生物。对水生受体产生不利影响的可能性取决于单个化合物和混合物的暴露方式和毒性。为了研究这些化合物的神经毒性,采用48小时急性和21天慢性大型水蚤生物测定是与CPF和CPFO独立进行的。急性生物测定结果表明,CPF和CPFO的中位致死浓度(LC50)为0.76μg/ L,CPFO的中位致死浓度(LC50)急性毒性为D. magna的2.4倍。急性测定结果还用于得出基准剂量水平,CPF为0.58μg/ L,CPFO为0.25μg/ L。然而,在相关的长期暴露下,这两种化合物均未引起对繁殖或生长的影响。由于D. magna很小,因此是一个相对敏感的物种,并且AChE抑制不良反应途径高度保守,因此在评估对水生受体的不良影响时可以谨慎地推断这些结果。1个