Effects of the molluscicidal agent GA-C13:0, a natural occurring ginkgolic acid, on snail mitochondria

Ginkgolic acids (GAs) from the leaves and sarcotesta of Ginkgo biloba L. represent a new kind of molluscicide agent. To date, the mechanism(s) for the observed molluscicidal activity remains largely unknown. Since GA-C13:0 has effectively inhibited snail mobility, we examined the effects of the compound on mitochondrial function and gene expression as compared to niclosamide. Snail mitochondrial damage induced by GAs was tested using transmission electron microscopy (TEM) and gene-expression profiling of five mitochondrial enzymes using real-time PCR. GA-C13:0 was found to have a pronounced effect on snail mitochondria with gross ultrastructural changes. In addition, GA-C13:0 was also found to inhibit the gene expression of four mitochondrial enzymes including cytochrome c oxidase, adenosine triphosphate (ATP) synthase, cytochrome b and dihydronicotinamide adenine dinucleotide (NADH) dehydrogenase. In contrast, niclosamide did not show such effects on mitochondrial function and gene expression, suggesting that the molluscicidal activity of GA-C13:0 and niclosamide differed. Our results imply that snail mitochondria are a potential target for the molluscicidal activity of ginkgolic acids.

Graphical abstractFigure optionsDownload full-size imageDownload as PowerPoint slideHighlights► GA-C13:0 had a pronounced effect on snail mitochondria with ultrastructural changes. ► GA-C13:0 could inhibit the gene expression of four mitochondrial enzymes. ► The molluscicidal activity of GA-C13:0 and niclosamide was different.