Volatile pesticides impair olfactory function in workers/farmers and insects, but data on molecular responses and mechanisms are poorly understood. This study aims to reveal the mechanisms of olfactory dysfunction in the silkworm after exposure to volatile dichlorvos. Our results demonstrated that acute exposure for 12 h significantly reduced electroantennogram responses, and over 62.50% of the treated male moths cannot locate the pheromone source. Transcriptional and proteomic responses of the antennae and heads were investigated. A total of 101 differentially expressed genes (DEGs) in the antennae, 138 DEGs in the heads, and 43 differentially expressed proteins (DEPs) in the heads including antennae were revealed. We discovered that upregulations of Arrestin1 and nitric oxide synthase1 (NOS1) may inhibit cyclic nucleotide-gated channels and hinder calcium influx in the antennae. In the central nervous systems (CNS), downregulations of tyrosine hydroxylase (TH) and tyrosine decarboxylase (TDC) may inhibit olfactory signal transduction by reducing the second messenger biosynthesis. Meanwhile, an abnormal increase of brain cell apoptosis was revealed by Annexin V-mCherry staining, often leading to persistent neurologic impairment. Taken together, this study highlighted olfactory dysfunction caused by dichlorvos, which may provide a novel perspective for understanding the toxicity mechanism of volatile pesticides in other organisms.

挥发性农药会损害工人/农民和昆虫的嗅觉功能，但对分子反应和机制的数据知之甚少。本研究旨在揭示家蚕接触挥发性敌敌畏后嗅觉功能障碍的机制。我们的研究结果表明，12 小时的急性暴露显着降低了触角电图反应，并且超过 62.50% 的经过处理的雄性飞蛾无法定位信息素来源。研究了触角和头部的转录和蛋白质组学反应。共揭示了101个触角差异表达基因（DEGs）、138个头部差异表达基因（DEGs）和43个包括触角在内的头部差异表达蛋白（DEPs）。我们发现Arrestin1和一氧化氮合酶1 的上调( NOS1 ) 可能抑制环状核苷酸门控通道并阻碍触角中的钙流入。在中枢神经系统 (CNS) 中，酪氨酸羟化酶( TH ) 和酪氨酸脱羧酶( TDC ) 的下调可能通过减少第二信使的生物合成来抑制嗅觉信号转导。同时，Annexin V-mCherry 染色显示脑细胞凋亡异常增加，通常导致持续性神经功能障碍。综上所述，本研究强调了敌敌畏引起的嗅觉功能障碍，这可能为了解挥发性农药对其他生物的毒性机制提供新的视角。