The mechanism of high-concentration florfenicol exposure inducing apoptosis in the midgut of Bombyx mori (Lepidoptera: Bombycidae)

The silkworm (Bombyx mori) is a Lepidoptera model insect, high concentrations of FF can impair the midgut physiological function, but the mechanism of action of which is still unclear. In this study, silkworms were continuously exposed to high concentrations (1.2 g/L) of FF for 72 h to investigate its mechanism of action. The results showed that FF exposure significantly inhibited the activity of key antioxidant enzymes, SOD, CAT, and TPX, in the midgut. Transmission electron microscopy revealed notable cellular damage, including microvilli shedding, chromatin aggregation, nuclear membrane depression, double membrane-bound vesicle autophagosomes, mitochondrial membrane rupture and swelling in the midgut after FF exposure. Furthermore, the oxidative phosphorylation pathway in the midgut was markedly suppressed, and the release of mitochondrial BmCytochrome c was significantly increased in the treatment group. The protein expression levels of BmCaspase-3 and cleaved BmCaspase-3 significantly were upregulated by 2.35-fold and 1.33-fold respectively, indicating the activation of the apoptotic signaling pathway. Additionally, TUNEL staining confirmed increased apoptotic signals in the midgut induced by FF. These findings suggest that high-concentration FF exposure triggers midgut apoptosis by reactive oxygen species (ROS) accumulation, which is the mechanism of physiological dysfunction in the midgut of silkworms. The research results provide a reference for evaluating the safety of high-concentration FF exposure in non-target organisms.