Cd exposure‐triggered toxicity in parasitic offspring of <i>Chouioia cunea</i> through <i>SLC24A3/SLC24A4</i> ‐apoptosis/oxidative damage signaling pathway

Heavy metals are widespread environmental pollutants. This study investigated the growth toxicity of cadmium (Cd) stress on Chouioia cunea offspring during the parasitism period within a Cd-contaminated food chain of artificial diets-Hyphantria cunea pupae-C. cunea. After parasitizing Cd-accumulated H. cunea pupae, the offspring exhibited a significant reduction in both body length and the expression levels of most growth regulatory genes. Transcriptome analysis revealed that, during the early parasitism stage, genes responsive to Cd stress predominantly involved the endoplasmic reticulum (ER) stress, mitochondrial dysfunction, apoptosis, and calcium homeostasis. In the subsequent stages of parasitism, Cd exposure induced substantial damage to the ER and mitochondrial ultrastructure, disrupted the antioxidant defense system, activated the mitochondrial apoptotic and ER stress pathways, and decreased the expression of SLC24A3 and SLC24A4. Overexpression of SLC24A3 and SLC24A4 in Sf9 cells mitigated Cd toxicity by alleviating the Ca²⁺-mitochondrial permeability transition pore (MPTP)-mitochondrial membrane potential (MMP) collapse/apoptosis and oxidative stress cascade reaction. Overall, Cd exposure impaired the growth of C. cunea parasitic offspring through the SLC24A3/SLC24A4-mediated apoptosis and oxidative damage signaling pathways.