NISCAIR Online Periodicals Repository

NISCAIR ONLINE PERIODICALS REPOSITORY (NOPR)  >
NISCAIR PUBLICATIONS >
Research Journals >
Indian Journal of Biochemistry and Biophysics (IJBB) >
IJBB Vol.49 [2012] >
IJBB Vol.49(5) [October 2012] >


Title: Role of CYP1A1 haplotypes in modulating susceptibility to coronary artery disease
Authors: Lakshmi, Sana Venkata Vijaya
Naushad, Shaik Mohammad
Saumya, Kankanala
Rao, Damera Seshagiri
Kutala, Vijay Kumar
Keywords: Coronary artery disease
One-carbon metabolism
Xenobiotic metabolism
8-Oxo-2' deoxyguanosine
CYP1A1 haplotypes
Issue Date: Oct-2012
Publisher: NISCAIR-CSIR, India
Abstract: To investigate the role of cytochrome P450 1A1 (CYP1A1) haplotypes in modulating susceptibility to coronary artery disease (CAD), a case-control study was conducted by enrolling 352 CAD cases and 282 healthy controls. PCR-RFLP, multiplex PCR, competitive ELISA techniques were employed for the analysis of CYP1A1 [m1 (T→C), m2 (A→G) and m4 (C→A)] haplotypes, glutathione-S-transferase (GST)T1/GSTM1 null variants and plasma 8-oxo-2’deoxyguanosine (8-oxodG) respectively. Two CYP1A1 haplotypes, i.e. CAC and TGC showed independent association with CAD risk, while all-wild CYP1A1 haplotype i.e. TAC showed reduced risk for CAD. All the three variants showed mild linkage disequilibrium (D’: 0.05 to 0.17). GSTT1 null variant also exerted independent association with CAD risk (OR: 2.53, 95% CI 1.55–4.12). Among the conventional risk factors, smoking showed synergetic interaction with CAC haplotype of CYP1A1 and GSTT1 null genotype in inflating CAD risk. High risk alleles of this pathway showed dose-dependent association with percentage of stenosis and number of vessels affected. Elevated 8-oxodG levels were observed in subjects with CYP1A1 CAC haplotype and GSTT1 null variant. Multiple linear regression model of these xenobiotic variants explained 36% variability in 8-oxodG levels. This study demonstrated the association of CYP1A1 haplotypes and GSTT1 null variant with CAD risk and this association was attributed to increased oxidative DNA damage.
Page(s): 349-355
CC License:  CC Attribution-Noncommercial-No Derivative Works 2.5 India
ISSN: 0975-0959 (Online); 0301-1208 (Print)
Source:IJBB Vol.49(5) [October 2012]

Files in This Item:

File Description SizeFormat
IJBB 49(5) 349-355.pdf98.9 kBAdobe PDFView/Open
 Current Page Visits: 313 
Recommend this item

 

National Knowledge Resources Consortium |  NISCAIR Website |  Contact us |  Feedback

Disclaimer: NISCAIR assumes no responsibility for the statements and opinions advanced by contributors. The editorial staff in its work of examining papers received for publication is helped, in an honorary capacity, by many distinguished engineers and scientists.

CC License Except where otherwise noted, the Articles on this site are licensed under Creative Commons License: CC Attribution-Noncommercial-No Derivative Works 2.5 India

Copyright © 2012 The Council of Scientific and Industrial Research, New Delhi. All rights reserved.

Powered by DSpace Copyright © 2002-2007 MIT and Hewlett-Packard | Compliant to OAI-PMH V 2.0

Home Page Total Visits: 509454 since 06-Feb-2009  Last updated on 11-Apr-2014Webmaster: nopr@niscair.res.in