Bisphenol A Modulates Autophagy and Exacerbates Chronic Kidney Damage in Mice.
Animals
Antioxidants
/ pharmacology
Apoptosis
/ drug effects
Autophagy
/ drug effects
Benzhydryl Compounds
/ adverse effects
Cell Line
Female
Humans
Kidney
/ metabolism
Kidney Diseases
/ metabolism
Kidney Tubules
/ drug effects
Male
Mice
Mice, Inbred C57BL
Oxidative Stress
/ drug effects
Phenols
/ adverse effects
Renal Insufficiency, Chronic
/ metabolism
Bisphenol A
autophagy
fibrosis
inflammation
oxidative stress
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
03 Jul 2021
03 Jul 2021
Historique:
received:
31
05
2021
revised:
28
06
2021
accepted:
29
06
2021
entrez:
20
7
2021
pubmed:
21
7
2021
medline:
27
7
2021
Statut:
epublish
Résumé
Bisphenol A (BPA) is a ubiquitous environmental toxin that accumulates in chronic kidney disease (CKD). Our aim was to explore the effect of chronic exposition of BPA in healthy and injured kidney investigating potential mechanisms involved. In C57Bl/6 mice, administration of BPA (120 mg/kg/day, i.p for 5 days/week) was done for 2 and 5 weeks. To study BPA effect on CKD, a model of subtotal nephrectomy (SNX) combined with BPA administration for 5 weeks was employed. In vitro studies were done in human proximal tubular epithelial cells (HK-2 line). Chronic BPA administration to healthy mice induces inflammatory infiltration in the kidney, tubular injury and renal fibrosis (assessed by increased collagen deposition). Moreover, in SNX mice BPA exposure exacerbates renal lesions, including overexpression of the tubular damage biomarker Hepatitis A virus cellular receptor 1 ( BPA deregulates autophagy flux and redox protective mechanisms, suggesting a potential mechanism of BPA deleterious effects in the kidney.
Sections du résumé
BACKGROUND
BACKGROUND
Bisphenol A (BPA) is a ubiquitous environmental toxin that accumulates in chronic kidney disease (CKD). Our aim was to explore the effect of chronic exposition of BPA in healthy and injured kidney investigating potential mechanisms involved.
METHODS
METHODS
In C57Bl/6 mice, administration of BPA (120 mg/kg/day, i.p for 5 days/week) was done for 2 and 5 weeks. To study BPA effect on CKD, a model of subtotal nephrectomy (SNX) combined with BPA administration for 5 weeks was employed. In vitro studies were done in human proximal tubular epithelial cells (HK-2 line).
RESULTS
RESULTS
Chronic BPA administration to healthy mice induces inflammatory infiltration in the kidney, tubular injury and renal fibrosis (assessed by increased collagen deposition). Moreover, in SNX mice BPA exposure exacerbates renal lesions, including overexpression of the tubular damage biomarker Hepatitis A virus cellular receptor 1 (
CONCLUSIONS
CONCLUSIONS
BPA deregulates autophagy flux and redox protective mechanisms, suggesting a potential mechanism of BPA deleterious effects in the kidney.
Identifiants
pubmed: 34281243
pii: ijms22137189
doi: 10.3390/ijms22137189
pmc: PMC8268806
pii:
doi:
Substances chimiques
Antioxidants
0
Benzhydryl Compounds
0
Phenols
0
bisphenol A
MLT3645I99
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
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