Alteration of intestinal microbiota-intestinal barrier interaction interferes with intestinal health after microcystin-LR exposure in Lithobates catesbeianus tadpoles.

There remains uncertainty regarding the influence of microcystin-leucine arginine (MC-LR) on amphibian intestinal health, specifically how MC-LR interferes with intestinal microbiota following exposure to environmental concentrations. In this study, Lithobates catesbeianus tadpoles were exposed to varying MC-LR concentrations (0, 0.5, and 2 µg/L) over a 30-day period. The aim was to investigate how altered interactions between tadpole intestinal microbiota and the intestinal barrier influence intestinal health following MC-LR exposure. Following exposure to the MC-LR at low ambient concentrations, tadpole intestinal tissue was damaged. It had increased permeability, reduced pathogen inhibition capacity, and impaired digestive function. Additionally, there was a significant increase in lipopolysaccharide content and upregulation of downstream response genes, including TLR4, MyD88, and NF-κB, within the intestinal tissue. Therefore, eosinophils' count and pro-inflammatory cytokines' expression increased. In addition, MC-LR exposure induced oxidative stress and mitochondrial structural damage by increasing the levels of reactive oxygen species in intestinal tissue. CytoC and Bax transcription, as well as caspase 9 and caspase 3 activities, increased significantly. Significant downregulation of Bcl-2 transcription promoted apoptosis in tadpole intestinal cells. MC-LR exposure disrupted intestinal microbiota and metabolism in tadpoles. Correlation analysis revealed a strong association between intestinal microbiota and oxidative stress, inflammation, immunity, and tissue damage in the intestine. Conclusively, this study provides the first demonstration that MC-LR significantly affects amphibian intestinal microbiota, highlighting tadpoles' susceptibility to environmental risks posed by MC-LR.