Long Term Perinatal Deltamethrin Exposure Alters Electrophysiological Properties of Embryonic Ventricular Cardiomyocyte.
Action Potentials
/ drug effects
Animals
Calcium Channels, L-Type
/ genetics
Cell Survival
/ drug effects
Disease Models, Animal
ERG1 Potassium Channel
Embryo, Mammalian
/ chemistry
Female
Gene Expression Regulation, Developmental
/ drug effects
Gestational Age
Humans
Maternal Exposure
/ adverse effects
Mice
Mortality
Myocytes, Cardiac
/ cytology
Nitriles
/ adverse effects
Potassium Channels, Inwardly Rectifying
/ genetics
Pregnancy
Pyrethrins
/ adverse effects
action potential
deltamethrin
developmental cardiotoxicity
embryonic cardiomyocytes
pyrethroid
Journal
Current medical science
ISSN: 2523-899X
Titre abrégé: Curr Med Sci
Pays: China
ID NLM: 101729993
Informations de publication
Date de publication:
Feb 2019
Feb 2019
Historique:
received:
30
04
2018
revised:
28
12
2018
entrez:
15
3
2019
pubmed:
15
3
2019
medline:
2
7
2019
Statut:
ppublish
Résumé
Increased use of pyrethroids and the exposure to pyrethroids for pregnant women and children have raised the concerns over the potential effect of pyrethroids on developmental cardiotoxicity and other abnormalities. The purpose of this study was to investigate whether long term perinatal deltamethrin exposure altered embryonic cardiac electrophysiology in mice. Pregnant mice were administered with 0 or 3 mg/kg of deltamethrin by gavage daily from gestational day (gd) 10.5 to gd 17. 5. Whole cell patch-clamp technique was used in electrophysiological study, and real time RT-PCR was applied to analyze the molecular changes for the electrophysiological properties. Deltamethrin exposure resulted in increased mortality of pregnant mice and decreased viability of embryos. Moreover, deltamethrin slowed the maximum depolarization velocity (Vmax), prolonged the action potential duration (APD) and depolarized the maximum diastolic potential (MDP) of embryonic cardiomyocytes. Additionally, perinatal deltamethrin exposure decreased the mRNA expression of Na
Identifiants
pubmed: 30868487
doi: 10.1007/s11596-019-1995-5
pii: 10.1007/s11596-019-1995-5
doi:
Substances chimiques
Calcium Channels, L-Type
0
ERG1 Potassium Channel
0
Kcnh2 protein, mouse
0
Kir2.1 channel
0
Nitriles
0
Potassium Channels, Inwardly Rectifying
0
Pyrethrins
0
decamethrin
2JTS8R821G
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
21-27Références
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