Impact of imidacloprid exposure on the biochemical responses, transcriptome, gut microbiota and growth performance of the Pacific white shrimp Litopenaeus vannamei

The widespread use of neonicotinoid insecticides, such as imidacloprid, in agriculture is one of the key factors for the drop in the survival of invertebrates, including decapod crustaceans. However, there is currently a lack of comprehensive studies on the chronic toxicity mechanisms in decapod crustaceans. Here, the concentration-dependent effects of imidacloprid on the physiology and biochemistry, gut microbiota and transcriptome of L. vannamei, and the interaction between imidacloprid, gut microbiota and genes were studied. Imidacloprid caused oxidative stress, leading to reduced growth and to immunity and tissue damage in L. vannamei. Imidacloprid increased the gut pathogenic microbiota abundance and broke the steady state of the gut microbiota interaction network, resulting in microbiota function disorders. Chronic imidacloprid exposure induced overall transcriptome changes in L. vannamei. Specifically, imidacloprid caused a large number of differentially expressed genes (DEGs) to be significantly downregulated. The inhibition of autophagy-related pathways revealed the toxic process of imidacloprid to L. vannamei. The changes in phase I and II detoxification gene expression clarified the formation of a detoxification mechanism in L. vannamei. The disturbance of circadian rhythm (CLOCK) caused by imidacloprid is one of the reasons for the increase in gut pathogenic microbiota abundance.