LAUSR

BACKGROUND Emamectin benzoate (EMB) is a semisynthetic bioinsecticide, which has been widely used in the control of forestry and agricultural pests. However, the mechanism of its toxic effects on the non-neural tissues has been rarely reported. Here, we explored the mechanism of the midgut damage induced by EMB in gypsy moth (Lymantria dispar) in order to better understand the toxicological mechanism of EMB. RESULTS Our results confirmed that EMB caused damage to midgut of gypsy moth by inducing apoptosis. Transcriptome showed that 1469, 650 and 950 genes were significantly differential expression in the midgut of gypsy moth after 24, 48 and 72 h of EMB exposure, and oxidative stress, energy metabolism disorder and apoptosis may be related to the toxic effects of EMB. The indicators related to oxidative stress, energy metabolism and apoptosis were further examined. The results showed that EMB could cause oxidative stress by increasing ROS level and inhibiting antioxidant enzymes (p < 0.05), such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), which in turn causes mitochondria injury. Subsequently, energy metabolism was inhibited by downregulating the activities and mRNA level of energy metabolism enzymes. Furthermore, the mitochondrial apoptosis pathway was activated, triggering apoptosis, and eventually causing midgut injury in gypsy moth. CONCLUSION Our results indicated that EMB caused damage to midgut by inducing oxidative stress, energy metabolism disorder and apoptosis in gypsy moth. Our findings shed new lights on the toxicological mechanism of EMB on non-neural tissues from oxidative stress, energy metabolism and apoptosis perspectives. This article is protected by copyright. All rights reserved.