Cadmium exposure triggers adaptive physiological and molecular responses that undermine development in Bactrocera...

The oriental fruit fly, Bactrocera dorsalis (Diptera: Tephritidae), an important invasive fruit and vegetable pest, exhibits a broad host range that includes citrus, mango, and banana. Its larvae bore into fruit tissues, causing severe economic losses. Cadmium (Cd²⁺) is classified among the most toxic heavy metal contaminants, capable of accumulating in plants and biomagnifying through food chains, thereby threatening biodiversity and human health. This study assessed the effects of Cd²⁺ stress on B. dorsalis larval growth and development, alongside changes in key enzymatic activities and transcriptional responses of metabolic pathways. Cd²⁺ exposure significantly inhibited growth and development in a concentration-dependent manner. Compared to controls, larvae exposed to 10 mg/L Cd²⁺ showed reductions in body weight of 1.88-3.73 mg, prolonged development by 2-7 days, and a 20%-40% decrease in survival. Adults exposed to 10 mg/L Cd²⁺ displayed significantly reduced fecundity. At 20 mg/L Cd²⁺, pupal weight declined by 5 mg, and adult eclosion rate dropped by 25%. In third-instar larvae, exposure to Cd10 (10 mg/L Cd²⁺) significantly increased the activities of superoxide dismutase (SOD), peroxidase (POD), and carboxylesterase (CarE) by 1.14-, 2.17-, and 1.72-fold, respectively, while markedly reducing catalase (CAT) activity to 44% of the control level. Comparative transcriptomic analysis revealed that Cd5 (5 mg/L Cd²⁺) treatment significantly upregulated genes involved in oxidative phosphorylation and ribosome pathways. Additionally, detoxification-related genes, such as ABC transporters and cytochrome P450, also exhibited substantial transcriptional changes. In conclusion, Cd²⁺ exposure impairs the growth and development, and physiology of B. dorsalis, driving changes in antioxidant and detoxification enzyme activities and triggering transcriptional responses in oxidative phosphorylation pathways. These findings also elucidate the molecular basis of Cd²⁺ stress adaptation in this species.