Luo, Hong-yan, Masika, Jacob, Guan, Xiu-wen, Nie, Li, Ao, Dong-hui, Qi, Yu, Shi, Rui, Hescheler, Juergen and Zeng, Ying (2019). Long Term Perinatal Deltamethrin Exposure Alters Electrophysiological Properties of Embryonic Ventricular Cardiomyocyte. Curr. Med. Sci., 39 (1). S. 21 - 28. NEW YORK: SPRINGER. ISSN 2523-899X

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Abstract

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+ channel regulatory subunit Nav1, inward rectifier K+ channel subunit Kir2.1, and delayed rectifier K+ channel subunit MERG while the L-type Ca2+ channel subunit, Cav1.2 expression was increased. On the contrary, deltamethrin administration did not significantly alter the regulation of -adrenergic or muscarinic receptor on embryonic cardiomyocytes. In conclusion, deltamethrin exposure at perinatal stage significantly alters mRNA expression of embryonic cardiac ion channels and therefore influences embryonic cardiac electrophysiological properties. This highlights the need to understand the persistent effects of pyrethroid exposure on cardiac function during embryonic development due to potential for cardiac arrhythmogenicity.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Luo, Hong-yanUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Masika, JacobUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Guan, Xiu-wenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Nie, LiUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ao, Dong-huiUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Qi, YuUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Shi, RuiUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Hescheler, JuergenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Zeng, YingUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-157256
DOI: 10.1007/s11596-019-1995-5
Journal or Publication Title: Curr. Med. Sci.
Volume: 39
Number: 1
Page Range: S. 21 - 28
Date: 2019
Publisher: SPRINGER
Place of Publication: NEW YORK
ISSN: 2523-899X
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
PYRETHROID INSECTICIDES; EARLY AFTERDEPOLARIZATIONS; CORD BLOOD; NEUROTOXICITY; FETAL; CYPERMETHRIN; PESTICIDES; CHANNEL; RATS; POPULATIONMultiple languages
Medicine, Research & ExperimentalMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/15725

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