Postnatal Smoke Exposure Further Increases the Hepatic Nicotine Metabolism in Prenatally Smoke Exposed Male Offspring and Is Linked with Aberrant <i>Cyp2a5</i> Methylation

Postnatal Smoke Exposure Further Increases the Hepatic Nicotine Metabolism in Prenatally Smoke Exposed Male Offspring and Is Linked with Aberrant <i>Cyp2a5</i> Methylation

Prenatal smoke exposure (PreSE) is a risk factor for nicotine dependence, which is further enhanced by postnatal smoke exposure (PostSE). One susceptibility gene to nicotine dependence is Cytochrome P450 (CYP) 2A6, an enzyme responsible for the conversion of nicotine to cotinine in the liver. Higher...

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Bibliographic Details
Main Authors: Khosbayar Lkhagvadorj, Zhijun Zeng, Karolin F. Meyer, Laura P. Verweij, Wierd Kooistra, Marjan Reinders-Luinge, Henk W. Dijkhuizen, Inge A. M. de Graaf, Torsten Plösch, Machteld N. Hylkema
Format: Article
Language:English
Published: MDPI AG 2021-12-01
Series:International Journal of Molecular Sciences
Subjects:
epigenetics
CYP2A5
sex-difference
nicotine addiction
postnatal smoke exposure
Online Access:https://www.mdpi.com/1422-0067/22/1/164

Internet

https://www.mdpi.com/1422-0067/22/1/164

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