Atorvastatin effect on the distribution of high-density lipoprotein subfractions and human paraoxonase activity

M. Harangi, Hossein Z. Mirdamadi, I. Seres, Ferenc Sztanek, M. Molnár, Andrea Kassai, Zoltán Derdák, László Illyés, G. Paragh

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Human serum paraoxonase-1 (PON1) protects lipoproteins against oxidation by hydrolyzing lipid peroxides in oxidized low-density lipoprotein (LDL); therefore, it may protect against atherosclerosis. Changes in the ratio of high-density lipoprotein (HDL) subfractions may alter the stability and the antioxidant capacity of PON1. The aim of the study was to examine the effect of atorvastatin treatment on the distribution of HDL subfractions, LDL size, cholesteryl ester transfer protein (CETP), lecithin-cholesterol acyltransferase (LCAT), and PON1 activity. In all, 33 patients with type IIa and IIb hypercholesterolemia were involved in the study. LDL sizes and HDL subfractions were determined by gradient gel electrophoresis. CETP, LCAT, and PON1 activities were measured spectrophotometrically. Three months of treatment with atorvastatin 20 mg daily significantly increased the HDL3 (+8.13%) and decreased the HDL2a and HDL2b subfractions (-1.57% and -6.55%, respectively). The mean LDL size was significantly increased (+3.29%). The level of oxidized LDL was significantly decreased (-46.0%). The PON1 activity was augmented by the atorvastatin treatment (+5.0%). The CETP activity positively correlated with the HDL2b level and negatively correlated with the HDL3 and HDL2a levels. Atorvastatin alters the HDL subfractions, which may improve its antiatherogenic effect via enhancement of the PON1 activity.

Original languageEnglish
Pages (from-to)190-198
Number of pages9
JournalTranslational Research
Volume153
Issue number4
DOIs
Publication statusPublished - Apr 2009

Fingerprint

Aryldialkylphosphatase
HDL Lipoproteins
Human Activities
Cholesterol Ester Transfer Proteins
LDL Lipoproteins
Phosphatidylcholine-Sterol O-Acyltransferase
Lipid Peroxides
Hypercholesterolemia
Lipoproteins
Electrophoresis
Atherosclerosis
Therapeutics
Antioxidants
Gels
Atorvastatin Calcium
Oxidation
Serum

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, medical
  • Public Health, Environmental and Occupational Health

Cite this

Atorvastatin effect on the distribution of high-density lipoprotein subfractions and human paraoxonase activity. / Harangi, M.; Mirdamadi, Hossein Z.; Seres, I.; Sztanek, Ferenc; Molnár, M.; Kassai, Andrea; Derdák, Zoltán; Illyés, László; Paragh, G.

In: Translational Research, Vol. 153, No. 4, 04.2009, p. 190-198.

Research output: Contribution to journalArticle

Harangi, M. ; Mirdamadi, Hossein Z. ; Seres, I. ; Sztanek, Ferenc ; Molnár, M. ; Kassai, Andrea ; Derdák, Zoltán ; Illyés, László ; Paragh, G. / Atorvastatin effect on the distribution of high-density lipoprotein subfractions and human paraoxonase activity. In: Translational Research. 2009 ; Vol. 153, No. 4. pp. 190-198.
@article{57296681e99242ea9f7e11c44d58697b,
title = "Atorvastatin effect on the distribution of high-density lipoprotein subfractions and human paraoxonase activity",
abstract = "Human serum paraoxonase-1 (PON1) protects lipoproteins against oxidation by hydrolyzing lipid peroxides in oxidized low-density lipoprotein (LDL); therefore, it may protect against atherosclerosis. Changes in the ratio of high-density lipoprotein (HDL) subfractions may alter the stability and the antioxidant capacity of PON1. The aim of the study was to examine the effect of atorvastatin treatment on the distribution of HDL subfractions, LDL size, cholesteryl ester transfer protein (CETP), lecithin-cholesterol acyltransferase (LCAT), and PON1 activity. In all, 33 patients with type IIa and IIb hypercholesterolemia were involved in the study. LDL sizes and HDL subfractions were determined by gradient gel electrophoresis. CETP, LCAT, and PON1 activities were measured spectrophotometrically. Three months of treatment with atorvastatin 20 mg daily significantly increased the HDL3 (+8.13{\%}) and decreased the HDL2a and HDL2b subfractions (-1.57{\%} and -6.55{\%}, respectively). The mean LDL size was significantly increased (+3.29{\%}). The level of oxidized LDL was significantly decreased (-46.0{\%}). The PON1 activity was augmented by the atorvastatin treatment (+5.0{\%}). The CETP activity positively correlated with the HDL2b level and negatively correlated with the HDL3 and HDL2a levels. Atorvastatin alters the HDL subfractions, which may improve its antiatherogenic effect via enhancement of the PON1 activity.",
author = "M. Harangi and Mirdamadi, {Hossein Z.} and I. Seres and Ferenc Sztanek and M. Moln{\'a}r and Andrea Kassai and Zolt{\'a}n Derd{\'a}k and L{\'a}szl{\'o} Illy{\'e}s and G. Paragh",
year = "2009",
month = "4",
doi = "10.1016/j.trsl.2009.01.007",
language = "English",
volume = "153",
pages = "190--198",
journal = "Translational Research",
issn = "1931-5244",
publisher = "Mosby Inc.",
number = "4",

}

TY - JOUR

T1 - Atorvastatin effect on the distribution of high-density lipoprotein subfractions and human paraoxonase activity

AU - Harangi, M.

AU - Mirdamadi, Hossein Z.

AU - Seres, I.

AU - Sztanek, Ferenc

AU - Molnár, M.

AU - Kassai, Andrea

AU - Derdák, Zoltán

AU - Illyés, László

AU - Paragh, G.

PY - 2009/4

Y1 - 2009/4

N2 - Human serum paraoxonase-1 (PON1) protects lipoproteins against oxidation by hydrolyzing lipid peroxides in oxidized low-density lipoprotein (LDL); therefore, it may protect against atherosclerosis. Changes in the ratio of high-density lipoprotein (HDL) subfractions may alter the stability and the antioxidant capacity of PON1. The aim of the study was to examine the effect of atorvastatin treatment on the distribution of HDL subfractions, LDL size, cholesteryl ester transfer protein (CETP), lecithin-cholesterol acyltransferase (LCAT), and PON1 activity. In all, 33 patients with type IIa and IIb hypercholesterolemia were involved in the study. LDL sizes and HDL subfractions were determined by gradient gel electrophoresis. CETP, LCAT, and PON1 activities were measured spectrophotometrically. Three months of treatment with atorvastatin 20 mg daily significantly increased the HDL3 (+8.13%) and decreased the HDL2a and HDL2b subfractions (-1.57% and -6.55%, respectively). The mean LDL size was significantly increased (+3.29%). The level of oxidized LDL was significantly decreased (-46.0%). The PON1 activity was augmented by the atorvastatin treatment (+5.0%). The CETP activity positively correlated with the HDL2b level and negatively correlated with the HDL3 and HDL2a levels. Atorvastatin alters the HDL subfractions, which may improve its antiatherogenic effect via enhancement of the PON1 activity.

AB - Human serum paraoxonase-1 (PON1) protects lipoproteins against oxidation by hydrolyzing lipid peroxides in oxidized low-density lipoprotein (LDL); therefore, it may protect against atherosclerosis. Changes in the ratio of high-density lipoprotein (HDL) subfractions may alter the stability and the antioxidant capacity of PON1. The aim of the study was to examine the effect of atorvastatin treatment on the distribution of HDL subfractions, LDL size, cholesteryl ester transfer protein (CETP), lecithin-cholesterol acyltransferase (LCAT), and PON1 activity. In all, 33 patients with type IIa and IIb hypercholesterolemia were involved in the study. LDL sizes and HDL subfractions were determined by gradient gel electrophoresis. CETP, LCAT, and PON1 activities were measured spectrophotometrically. Three months of treatment with atorvastatin 20 mg daily significantly increased the HDL3 (+8.13%) and decreased the HDL2a and HDL2b subfractions (-1.57% and -6.55%, respectively). The mean LDL size was significantly increased (+3.29%). The level of oxidized LDL was significantly decreased (-46.0%). The PON1 activity was augmented by the atorvastatin treatment (+5.0%). The CETP activity positively correlated with the HDL2b level and negatively correlated with the HDL3 and HDL2a levels. Atorvastatin alters the HDL subfractions, which may improve its antiatherogenic effect via enhancement of the PON1 activity.

UR - http://www.scopus.com/inward/record.url?scp=62649094401&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=62649094401&partnerID=8YFLogxK

U2 - 10.1016/j.trsl.2009.01.007

DO - 10.1016/j.trsl.2009.01.007

M3 - Article

C2 - 19304278

AN - SCOPUS:62649094401

VL - 153

SP - 190

EP - 198

JO - Translational Research

JF - Translational Research

SN - 1931-5244

IS - 4

ER -