Sublethal chlorantraniliprole exposure induces autophagy and apoptosis through disrupting calcium homeostasis in the silkworm <scp> <i>Bombyx mori</i> </scp>

Abstract

Abstract The intensive application of chlorantraniliprole (CAP) leaves residues in the environment, posing a potential threat to non‐target organisms. In the present study, we investigated the adverse effects of sublethal CAP exposure on Bombyx mori . Sublethal CAP (0.02 mg/L) was shown to induce the release of intracellular Ca 2+ in BmN cells. Meanwhile, Ca 2+ ‐dependent genes were induced in the midgut at 72 h after CAP (0.01 mg/L) exposure, and damaged mitochondria, autophagosomes, nuclear membrane rupture and condensed chromatin were observed. Moreover, the key genes in the oxidative phosphorylation pathway were significantly down‐regulated. The transcript levels of autophagy‐related genes ATG6 and ATG8 were significantly up‐regulated, and the protein levels of LC3‐II and ATG7 were significantly increased by 3.72‐ and 3.33‐fold, respectively. Additionally, the transcript levels of the upstream genes in the apoptosis pathway ( calpain and Apaf‐1 ) were significantly up‐regulated, the protein levels of the downstream gene caspase 3 and its cleaved form were significantly up‐regulated by 1.97‐ and 4.55‐fold, respectively, consistent with the elevated caspase 3 activity at 72 h. Collectively, these findings demonstrate that intracellular Ca 2+ release induced by sublethal CAP inhibits oxidative phosphorylation pathway, which causes mitochondrial dysfunction, leading to autophagy and apoptosis in the midgut of B. mori .

Topics & Concepts