Study effect and mechanism of levofloxacin on the neurotoxicity of Rana nigromaculata tadpoles exposed to imidacloprid based on the microbe-gut-brain axis

Abstract

Aquatic organisms may be simultaneously exposed to antibiotics and pesticides. After levofloxacin (LVFX), imidacloprid (IMI) exposure and co-exposure at environmental levels, we found LVFX and IMI had antagonistic effect on the neurotoxicity of tadpoles. IMI-induced neurotoxicity on tadpoles can be explained by oxidative stress and hormone levels in some degree. By regulating ornithine, l-asparagine, putrescine and tryptamine in the intestine, LVFX affected glutathione metabolism, arginine and proline metabolism, alanine, aspartate and glutamate metabolism, tyrosine metabolism and aminoacyl tRNA biosynthesis, so then eased the neurotoxicity caused by IMI. More interestingly, Fusobacteriota and Cetobacterium might play an important role on easing the neurotoxicity caused by IMI. In addition, LVFX might have a laxation effect on the increased relative abundance of Bacteroidota caused by IMI. In conclusion, IMI not only affected oxidative stress and hormone levels in the brain, but also affected the synthesis of neurotransmitters in the intestine by regulating intestinal microbiota. In LVFX and IMI co-exposed groups, LVFX alleviated the neurotoxicity caused by IMI through regulating the intestinal microbiota, showing as an antagonistic effect. Our results provided a new perspective for aquatic ecological risk assessment under co-exposure of antibiotics and pesticides.

Keywords: Behavior endpoint; Co-exposure; Intestinal microbiota; Juvenile amphibians; Neurotransmitter metabolites.