Atorvastatin preferentially reduces LDL-associated platelet-activating factor acetylhydrolase activity in dyslipidemias of type IIA and type IIB (Journal article)
Tsimihodimos, V./ Karabina, S. A. P./ Tambaki, A. P./ Bairaktari, E./ Goudevenos, J. A./ Chapman, M. J./ Elisaf, M./ Tselepis, A. D.
Human plasma platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A(2) that is primarily associated with low density lipoprotein (LDL). PAF-AH activity has also been found in high density lipoprotein (HDL), although it has recently been indicated that there is no PAF-AH protein in HDL. Plasma paraoxonase 1 (PON1) is an HDL-associated esterase, which also exhibits PAF-AH-like activity. The effect of atorvastatin (20 mg per day for 4 months) on PAF-AH and PON1 activities in patients with dyslipidemia of type IIA (n=55) or type IIB (n=21) was studied. In both patient groups, atorvastatin significantly reduced plasma PAF-AH activity because of the decrease in LDL plasma levels and the preferential decrease in PAF-AH activity on dense LDL subfractions (LDL-4 and LDL-5). Drug therapy did not affect HDL-associated PAF-AH activity or serum PON1 activities toward paraoxon and phenylacetate in either patient group. However, because of the reduction in LDL cholesterol levels, the ratios of HDL-associated PAF-AH and serum PON1 activities to LDL cholesterol levels were significantly increased after drug administration. The reduction of the LDL-associated PAF-AH activity and the elevation in the ratios of HDL-associated PAF-AH and PON1 activities to LDL plasma levels may represent a new dimension in the antiatherogenic effect of atorvastatin.
|Institution and School/Department of submitter:||Πανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείας|
|Keywords:||hyperlipidemia,monocytes/macrophages,platelet-activating factor acetylhydrolase,paraoxonase,atorvastatin,low-density-lipoprotein,dependent diabetes-mellitus,human-plasma,familial hypercholesterolemia,paraoxonase activity,paf-acetylhydrolase,phospholipase a(2),coronary heart,oxidation,therapy|
|Link:||<Go to ISI>://000173786600017|
|Publisher:||American Heart Association, Inc.|
|Appears in Collections:||Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)|
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