Fumonisins are a type of mycotoxin produced by Fusarium spp., mainly F. proliferatum and F. vertieilliodes, and represent a potential hazard to the health of animals and human beings. The toxicity and mechanism of action of fumonisins is ambiguous, and it is unclear whether fumonisins are toxic to insect cells. This study examines the toxicity of fumonisin B1 (FB1) and its mechanism of action in the Spodoptera frugiperda Sf9 cell line. We found that FB1 inhibited Sf9 cellular proliferation and arrested cell growth at the G2/M phase. Morphological observation showed that FB1 induced swelling, vacuole formation, and loss of adhesion in Sf9 cells. Flow cytometry analysis showed that FB1 caused depolarization of the cell membrane potential and hyperpolarization of the mitochondrial membrane potential. To uncover potential genes associated with the molecular mechanisms of FB1, 41 differentially expressed genes were identified by transcriptome analyses after FB1 treatment. These genes are putatively involved in detoxification metabolism, insect hormone regulation, cell apoptosis, and other related processes. Finally, six differentially expressed genes were chosen and validated by quantitative real-time PCR (QRT-PCR). Our test could provide a reference for other kinds of insect cells studies on FB1 stress. At the same time, our studies try to provide a possible for FB1 as a precursor compounds of biological insecticide.
Keywords: Fumonisin B(1); Genes; Sf9 cell lines; Toxicity.
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