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Beschreibung des Verlags

Human serum paraoxonase (aryldialkylphosphatase, EC; PON1) and human serum platelet-activating factor acetylhydrolase (1-alkyl-2-acetyl-glycero-phosphocholine esterase, 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetohydrolase, EC; PAF-AH) are associated with HDL [1, 2]. PAF-AH is also found in LDL and lipoprotein(a) [Lp(a)] [3]. Recently, paraoxonase and PAF-AH have been shown to inhibit the oxidative modification of LDL [4, 5]. Furthermore, paraoxonase and PAF-AH can destroy active lipids in mildly oxidized LDL and hence may protect against the induction of inflammatory responses in arterial wall cells [6, 7]. Oxidation of LDL is recognized as a key early stage in the development of atherosclerosis, leading to uptake of LDL by the macrophage scavenger receptor and hence to formation of foam cells [8]. Thus, there is the potential for HDL-associated paraoxonase and PAF-AH to directly inhibit these processes. The PON1 gene has two common polymorphisms at amino acids 55 and 192 [9]. The 192 polymorphism leads to a Glu[right arrow]Arg substitution and results in two different isoforms that have high and low activity towards paraoxon as substrate [9, 10]. It has been suggested that paraoxonase and PAF-AH work in concert to detoxify lipid peroxides in LDL and may therefore have antiatherogenic properties [6]. Patients with chronic renal failure are at a greatly increased risk of developing cardiovascular disease. This is only partly explained by an increased prevalence of conventional risk factors [11, 12]. Increased susceptibility of LDL to oxidation has been reported in chronic renal failure [13, 14], although other studies have failed to confirm this finding [15, 16]. In view of the ability of HDL to protect LDL against oxidation, the aim of our study was therefore to investigate the activities of serum paraoxonase/arylesterase and PAF-AH in patients with chronic renal failure and hence to assess whether changes in activity might contribute to the accelerated development of atherosclerosis.

Wissenschaft und Natur
1. Januar
American Association for Clinical Chemistry, Inc.

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