Imidacloprid-Induced Developmental Delay in Bee Larvae: A Study on the Roles of Molting Hormones and Acetylcholinesterase

Insect molting and morphological remodeling are regulated by periodic hormones, namely JH and 20E. While 20E promotes pupation, JH maintains juvenile characteristics and prevents metamorphosis by antagonizing the actions of 20E. This study investigated the developmental regulatory pathways of bee larvae and found that imidacloprid inhibited the expression of JHAMT, a positive regulator of JH synthesis. However, JH titer levels remained unaffected, indicating that the antagonistic effect of JH still restricts the molting process, maintaining the larval morphology. Imidacloprid toxicity led to a reduced 20E titer and Br-c expression, thereby blocking molting. Additionally, a decrease in 20E levels was accompanied by a decrease in AChE activity, which is known to cause delayed pupation and developmental arrest in insect larvae. Our results suggest that imidacloprid neurotoxicity may cause developmental delay in bee larvae by inhibiting the molting hormone 20E. Correlation analysis showed that decreases in 20E titer, Br-c expression, and AChE activity were positively correlated with decreased developmental rates, growth index, weight, and width growth.