Imidacloprid disrupts the endocrine system by interacting with androgen receptor in male mice.
Androgen receptor
Endocrine disruption
Imidacloprid
Molecular docking
Journal
The Science of the total environment
ISSN: 1879-1026
Titre abrégé: Sci Total Environ
Pays: Netherlands
ID NLM: 0330500
Informations de publication
Date de publication:
15 Mar 2020
15 Mar 2020
Historique:
received:
29
07
2019
revised:
16
10
2019
accepted:
23
10
2019
pubmed:
30
11
2019
medline:
26
3
2020
entrez:
30
11
2019
Statut:
ppublish
Résumé
In the current study, six-week-old male ICR mice were administered imidacloprid (IMI) at concentrations of 3, 10 and 30 mg/L for a duration of 10 weeks to investigate the toxicity of IMI on the endocrine system. We observed that testicular morphology was severely impaired and damaged, and the levels of serum testosterone (T) and the expression of androgen receptor (AR) decreased significantly. Molecular docking analysis suggested that IMI docks into the active site of AR successfully and that three key hydrogen bonds were formed with the active site residues Glu11, Gln41 and Lys138. The binding free energy value of the AR-IMI complex suggested a stable binding between IMI and AR. All these results indicated that IMI could interact with AR. In addition, major genes in the testis involved in the synthesis of cholesterol and T were generally inhibited, and the serum cholesterol sources were also reduced. Moreover, the aromatase in male mice was lacking after subchronic IMI exposure. The data acquired from the present study indicated that IMI could lead to endocrine disruption by interacting with AR and influence the expression of genes involved in the production of T in male mice.
Identifiants
pubmed: 31780179
pii: S0048-9697(19)35155-1
doi: 10.1016/j.scitotenv.2019.135163
pii:
doi:
Substances chimiques
Neonicotinoids
0
Nitro Compounds
0
Receptors, Androgen
0
imidacloprid
3BN7M937V8
Testosterone
3XMK78S47O
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
135163Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.