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Published by : PROFESSIONAL MEDICAL PUBLICATIONS |
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ISSN 1681-715X |
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ORIGINAL ARTICLE |
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Volume 24 |
April - June 2008 (Part-I) |
Number 2 |
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Apolipoprotein E polymorphism, paraoxonase-1
activity and coronary artery disease: is there a link
F. Nabatchian1, Sh. Khaghani2, R. Miri3, M. Mahmoodi4, A. Karimi5, P. Pasalar6
ABSTRACT
Objective: The association of ApoE allele frequencies with coronary artery disease (CAD) remains unknown in developing countries. Paraoxonase 1 (PON1) is an enzyme that is associated with high density lipoprotein (HDL) and hydrolyzes oxidized lipids in oxidized low density lipoprotein (LDL) and thus protects against the development of atherosclerosis. In this study the association of apoE polymorphism and PON1 with premature CAD was determined.
Methodology: The frequency of apo E alleles and the activity of the PON1 among 162 patients with early and late onset CAD was examined.
Results: The mean age in the early and late-onset groups were 44.9 ± 4.9 and 71.7±2.5 years respectively. Patients with early-onset CAD had significantly lower serum levels of HDL-C and higher LDL-C/HDL-C ratio than the late-onset group. There was no difference in serum levels of triglyceride, total cholesterol and LDL-C between the two groups. The e2 allele was significantly higher in the late-onset group. 35.0% of early-onset and 17.5% of late-onset group had low level of PON1. 86% of the early-onset CAD and all of the late-onset CAD patients with e3/ e4 genotype, had low or moderate level of PON1 activity.
Conclusion: We found a positive association between PON1 activity, HDL level and the onset of CAD. Our study suggests that there are modest associations between CAD and apo E alleles and that the lower activity of PON1 in the presence of lower apo E level may increase the susceptibility to early-onset CAD.
KEY WORDS:
Paraoxonase, Atherosclerosis, Early-onset coronary artery disease, Apolipoprotein E polymorphism, Lipid peroxidation, Oxidative stress, Antioxidant.Pak J Med Sci April - June 2008 (Part-I) Vol. 24 No. 2 204-208
1. F. Nabatchian,
2. Sh. Khaghani,
3. P. Pasalar,
Department of Biochemistry,
4. R. Miri,
Hospital of Imam Hossein,
Shahid Beheshti University of Medical Sciences,
Tehran, Iran,
5. M. Mahmoodi,
Amiraalam Hospital,
1-3,5: Tehran University of Medical Sciences,
Tehran, Iran.
6. Karimi A,
Tehran Heart Center,
Tehran, Iran.
Correspondence
Parvin Pasalar, Ph.D
Clinical Biochemistry, Dept. of Biochemistry
Faculty of Medicine,
Tehran University of Medical Sciences,
Tehran, Iran
E-mail: pasalar@tums.ac.ir
* Received for Publication: December 9, 2007
* Revision Received: February 14, 2007
* 2nd Revision Received: September 29, 2007
* Final Revision Accepted: December 25, 2007
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