Imidacloprid disturbed the gut barrier function and interfered with bile acids metabolism in mice. (November 2020)

• Record Type: Journal Article
• Authors: Yang, Guiling; Yuan, Xianling; Jin, Cuiyuan; Wang, Dou; Wang, Yanhua; Miao, Wenyu; Jin, Yuanxiang
• Is Part Of: Environmental pollution. Volume 266:Part 1(2020)
• Publication Date: 2020-11
• Subjects: Imidacloprid -- Liver injury -- Bile acids -- Gut barrier -- Gut microbiota; CA Cholic Acid -- LCA Lithocholic Acid -- DCA Deoxycholic Acid -- UDCA Ursodeoxycholic Acid -- CDCA Chenodeoxycholic Acid -- TCA Taurocholic Acid -- GCA Glycocholic Acid -- TLCA Taurolithocholate Acid -- GLCA Glycolithocholic Acid -- TDCA Taurodeoxycholate Acid -- TUDCA Tauroursodeoxycholate Acid -- TCDCA Taurochenodeoxycholate Acid -- GDCA Glycodeoxycholate Acid -- GCDCA Glycochenodeoxycholate Acid -- GUDCA Glycoursodeoxycholic Acid -- ALT alanine aminotransferase -- AST aspartate aminotransferase -- ALP alkaline phosphatase -- Sod1 superoxide dismutase 1 -- Cat catalase -- Gpx1 glutathione peroxidase 1 -- Gpx2 glutathione peroxidase 2 -- Gsta1 glutathione-S-transferase A1 -- Gss glutathione synthetase -- Gr glutathione reductase -- Ho-1 heme oxygenase 1 -- Cyp7a1 cholesterol 7a-hydroxylase -- Cyp8b1 sterol 12α-hydroxylase -- Cyp27a1 sterol 27-hydroxylase -- Cyp7b1 oxysterol 7α-hydroxylase -- Slc27a5 solute carrier family 27 member 5 -- Baat bile acid CoA, amino acid N-acyltransferase -- Bsep bile salt export pump -- Mrp2 multi drug resistance associated protein 2 -- Mrp3 multi drug resistance associated protein 3 -- Ntcp Na + taurocholate cotransporting peptide -- Fxr farnesoid X receptor -- Shp small heterodimer partner -- Asbt the apical sodium-dependent bile acid transporter -- Ostα Organic solute transporters α -- Ostβ organic solute transporters β -- I-babp ileal bile acid binding protein -- Fgf15 fibroblast growth factor 15 -- Muc1 mucin 1 -- Muc2 mucin 2 -- Muc3 mucin 3 -- Klf4 kruppel-like factor 4 -- Defa3 alpha-defensin 3 -- Defa20 alpha-defensin 20 -- Pla2g4a phospholipase A2, Group IIA -- Mmp-7 matrix metalloproteinase-7 -- Amg4 amtolmetin guacyl 4 -- Reg3 regenerating gene -- Lyz lysozyme -- Ano1 anoctamin 1 -- Nkcc1 Na-K-2Cl cotransporter 1 -- Cftr cystic fibrosis transmembrane conductance regulator -- Slc26A3 solute carrier family 26 member 3 -- Slc26A6 solute carrier family 26 member 6 -- Nhe3 sodium-hydrogen exchanger 3 -- Zo-1 zonula occludens-1; Pollution -- Periodicals; Pollution -- Environmental aspects -- Periodicals; Environmental Pollution -- Periodicals; Pollution -- Périodiques; Pollution -- Aspect de l'environnement -- Périodiques; Pollution -- Effets physiologiques -- Périodiques; Pollution; Pollution -- Environmental aspects; Periodicals; Electronic journals; 363.73
• DOI: 10.1016/j.envpol.2020.115290
• Languages: English
• ISSNs: 0269-7491

Abstract

Abstract: The toxicity of neonicotinoid insecticide imidacloprid (IMI) to mammals has recently received increasing attention. However, the effects of IMI on the gut barrier and liver function of male C57BL/6J mice are still unknown. The study showed that exposure to IMI could reduce relative liver weights, change hepatic tissue morphology and induce hepatic oxidative stress. The gut barrier function was greatly impaired by IMI exposure, which might increase the body's susceptibility to harmful substances in the gut. Meanwhile, the synthesis and metabolism of hepatic bile acids (BAs) was also affected by IMI exposure. The levels of serum and hepatic total bile acids (TBAs) decreased; in contrast, the fecal TBA levels increased after exposure to 30 mg/L IMI for 10 weeks. Sequencing of colonic contents revealed that the operational taxonomic units (OTUs) and α-diversity index increased and that the gram-negative bacteria overgrew, indicating that the balance of the gut microbiota was disrupted. The present study indicated that subchronic exposure to IMI interfered with the gut barrier function, interfering with BAs metabolism and causing gut microbiota imbalance in male C57BL/6J mice. Taken together, IMI residues appear to be potentially toxic to mammals and even humans. Graphical abstract: Image 1 Highlights: Subchronic imidacloprid exposure impaired the function of the gut barrier in male C57BL/6J mice. Subchronic exposure of imidacloprid induced gut microbiota imbalance in mice. Subchronic exposure of imidacloprid interfered with bile acids metabolism. Imidacloprid induced liver injury may be the direct reason for bile acids metabolism. Abstract : The present study reported that subchronic exposure to imidacloprid disturbed with the gut barrier function, interfering with BAs metabolism and causing gut microbiota imbalance in mice.