Effects and mechanisms of Bisphenol G on the neurobehavior of zebrafish
This work evaluated the chronic toxic target and mechanism of bisphenol G(BPG)toward adult zebrafish through chronic exposure.The results showed that BPG exposure resulted in abnormal behavior of zebrafish.In the 50µg/L BPG exposure group,the zebrafish moving distance and switching frequency between the upper and lower zones were significantly reduced,and the accumulative time at the bottom was increased by 22.7％.Both Sand 50μg/L exposures significantly changed the social behavior of zebrafish,with increased social distance by(126.8％and 151.2％of control,respectively),reduced contact time(80.1％and 73.7％of control,respectively),and showed significant anxiety-like behavior and cognitive impairment.Section staining showed injured brain structure and intestinal villi,as well as increased intestinal goblet cell and mucus secretion,indicating potential intestinal inflammation and the development of neurological diseases.Further targeted metabolomics revealed disordered levels of neurotransmitters in the gut and brain,with significant changes in levels of tryptophan,GABA,glutamine,norepinephrine,choline,and histamine.Enrichment analysis of the KEGG pathway showed that phenylalanine,tyrosine and tryptophan biosynthesis;valine,leucine and isoleucine biosynthesis;arginine biosynthesis and phenylalanine metabolism were mainly affected pathways and with gender discriminations.These pathways regulate zebrafish behavior by interfering with the transport and homeostasis of neurotransmitters.In conclusion,BPG induced significant neurobehavioral toxicity and neurotransmitter disorder in the brain and intestine of zebrafish,and the gut-brain axis may be involved in mediating this effect.
万方数据
维普
