Serious environmental pollution in the ecosystem makes phytophagous insects face a great risk of exposure to pollutants, especially heavy metals. This study aims to understand the effects of Cd exposure on the growth and development of Hyphantria cunea and to elucidate the mechanism of growth toxicity induced by Cd from the perspective of food utilization and energy metabolism. Our results showed that the larval basal growth data, growth index, fitness index, and standard growth index were significantly decreased after feeding on Cd-containing artificial diets. The Cd-treated larvae had significantly higher digestibility than the untreated larvae. However, the food consumption, efficiency of conversion of digested food, and efficiency of conversion of ingested food were significantly lower than those of untreated larvae. Eight key metabolites in the glycolysis pathway and six key metabolites in the tricarboxylic acid cycle pathway were significantly reduced in Cd-treated larvae. The mRNA expression levels of two regulatory genes (6-phosphofructokinase 1 and hexokinase-1) belonging to two key enzymes in the glycolysis pathway and four regulatory genes (isocitrate dehydrogenase-1, isocitrate dehydrogenase-3, citrate synthase, and oxoglutarate dehydrogenase) belonging to three key enzymes in the tricarboxylic acid cycle pathway were significantly lower in the Cd-treated group than in the control group. Furthermore, most fitness-related traits were significantly and positively correlated with food utilization (except approximate digestibility) or energy metabolism parameters. Taken together, Cd exposure-triggered growth retardation of H. cunea larvae is a consequence of disturbances in food utilization and energy metabolism, thereby emphasizing the toxicity of heavy metals.
Keywords: Environmental pollution; Growth retardation; Hyphantria cunea larvae; Toxicity.
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.