Study on the toxicity and action mechanism of diquat on Caenorhabditis elegans

Diquat (DQ), a contact herbicide extensively utilized in both agricultural and non-agricultural domains, exhibits a high correlation with neuronal disorders. Nevertheless, the toxicity and underlying mechanisms associated with exposure to environmental concentrations of DQ remain ambiguous. Here, we report a dose-dependent cellular neurotoxicity of DQ in C. elegans. Firstly, DQ significantly compromised the development and brood size of worms, shortened the lifespan, and caused epidermal abnormalities. An unbiased transcriptomic analysis disclosed several pathways related to cell death and peroxisome homeostasis underlying this organismal-level toxicity. Moreover, the exposure of DQ to C. elegans led to a notable increase of embryonic cell death. Concurrently, DQ exposure specifically caused the loss of dopamine neurons but not two types of neurons in adulthood, which is in accordance with DQ-induced muscle-related defects such as pharyngeal pumping, body bends, and head thrashes. Overall design: Wild-type N2 Caenorhabditis elegans were exposed to 0 and 100.00 µg/L DQ dibromide monohydrate solution (Tanmo Quality Inspection Technology Co., Jiangsu, China) at a constant temperature of 20°C for 72 hours. Samples were collected for transcriptional level analysis, with the untreated 0 µg/L DQ-exposed C. elegans used as the control. In the document, control-1, control-2, and control-3 represent the three replicates for the 0 µg/L DQ treatment, while treatment-1, treatment-2, and treatment-3 represent the three replicates for the 100.00 µg/L DQ treatment.