Department of Physiological Sciences, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK 74075, USA.
Toxicol Appl Pharmacol. 2010 Oct 15;248(2):144-55. doi: 10.1016/j.taap.2010.07.026. Epub 2010 Aug 5.
Chlorpyrifos (CPF) is a widely used organophosphorus insecticide (OP) and putative developmental neurotoxicant in humans. The acute toxicity of CPF is elicited by acetylcholinesterase (AChE) inhibition. We characterized dose-related (0.1, 0.5, 1 and 2mg/kg) gene expression profiles and changes in cell signaling pathways 24h following acute CPF exposure in 7-day-old rats. Microarray experiments indicated that approximately 9% of the 44,000 genes were differentially expressed following either one of the four CPF dosages studied (546, 505, 522, and 3,066 genes with 0.1, 0.5, 1.0 and 2.0mg/kg CPF). Genes were grouped according to dose-related expression patterns using K-means clustering while gene networks and canonical pathways were evaluated using Ingenuity Pathway Analysis®. Twenty clusters were identified and differential expression of selected genes was verified by RT-PCR. The four largest clusters (each containing from 276 to 905 genes) constituted over 50% of all differentially expressed genes and exhibited up-regulation following exposure to the highest dosage (2mg/kg CPF). The total number of gene networks affected by CPF also rose sharply with the highest dosage of CPF (18, 16, 18 and 50 with 0.1, 0.5, 1 and 2mg/kg CPF). Forebrain cholinesterase (ChE) activity was significantly reduced (26%) only in the highest dosage group. Based on magnitude of dose-related changes in differentially expressed genes, relative numbers of gene clusters and signaling networks affected, and forebrain ChE inhibition only at 2mg/kg CPF, we focused subsequent analyses on this treatment group. Six canonical pathways were identified that were significantly affected by 2mg/kg CPF (MAPK, oxidative stress, NFΚB, mitochondrial dysfunction, arylhydrocarbon receptor and adrenergic receptor signaling). Evaluation of different cellular functions of the differentially expressed genes suggested changes related to olfactory receptors, cell adhesion/migration, synapse/synaptic transmission and transcription/translation. Nine genes were differentially affected in all four CPF dosing groups. We conclude that the most robust, consistent changes in differential gene expression in neonatal forebrain across a range of acute CPF dosages occurred at an exposure level associated with the classical marker of OP toxicity, AChE inhibition. Disruption of multiple cellular pathways, in particular cell adhesion, may contribute to the developmental neurotoxicity potential of this pesticide.
毒死蜱(CPF)是一种广泛使用的有机磷杀虫剂(OP),也是人类潜在的发育神经毒物。CPF 的急性毒性是通过乙酰胆碱酯酶(AChE)抑制引起的。我们描述了在 7 日龄大鼠中,急性 CPF 暴露 24 小时后,与剂量相关(0.1、0.5、1 和 2mg/kg)的基因表达谱和细胞信号通路的变化。微阵列实验表明,在研究的四种 CPF 剂量(0.1、0.5、1.0 和 2.0mg/kg CPF)中,大约有 9%的 44000 个基因的表达存在差异(546、505、522 和 3066 个基因)。使用 K-均值聚类根据剂量相关的表达模式对基因进行分组,同时使用 Ingenuity Pathway Analysis®评估基因网络和经典途径。鉴定了 20 个簇,通过 RT-PCR 验证了选定基因的差异表达。四个最大的簇(每个簇包含 276 到 905 个基因)构成了所有差异表达基因的 50%以上,并且在暴露于最高剂量(2mg/kg CPF)时表现出上调。受 CPF 影响的基因网络总数也随着 CPF 的最高剂量急剧增加(0.1、0.5、1 和 2mg/kg CPF 分别为 18、16、18 和 50)。前脑胆碱酯酶(ChE)活性仅在最高剂量组显著降低(26%)。基于差异表达基因中剂量相关变化的幅度、受影响的基因簇和信号网络的相对数量以及仅在 2mg/kg CPF 时的前脑 ChE 抑制,我们将后续分析集中在该治疗组。鉴定出 6 条显著受 2mg/kg CPF 影响的经典途径(MAPK、氧化应激、NFΚB、线粒体功能障碍、芳香烃受体和肾上腺素能受体信号转导)。对差异表达基因的不同细胞功能的评估表明,与嗅觉受体、细胞粘附/迁移、突触/突触传递和转录/翻译相关的变化。在所有四个 CPF 给药组中,有 9 个基因受到不同程度的影响。我们得出结论,在一系列急性 CPF 剂量下,新生前脑中与有机磷毒性的经典标志物 AChE 抑制相关的最显著、一致的差异基因表达变化发生在与农药发育神经毒性潜力相关的暴露水平。多种细胞途径的破坏,特别是细胞粘附,可能导致这种杀虫剂的发育神经毒性。