Paraoxonase 1 and platelet-activating factor acetylhydrolase activities in patients with low hdl-cholesterol levels with or without primary hypertriglyceridemia.
BACKGROUND
Previous studies have shown that high density lipoprotein (HDL)-deficient states are associated with reduced paraoxonase 1 (PON1) activity. However, HDL reduction caused by primary hypertriglyceridemia has not been fully explored. The aim of the present study was to evaluate whether PON1 and platelet-activating factor acetylhydrolase (PAF-AH), two antioxidant enzymes, were altered in patients with low HDL-cholesterol levels with or without primary hypertriglyceridemia in comparison with control normolipemic subjects.


METHODS
We studied 24 patients with low HDL-cholesterol levels with (n=12) or without (n=12) primary hypertriglyceridemia in comparison with 12 control subjects who presented normal HDL-cholesterol and triglyceride levels. Paraoxon and phenylacetate were used as substrate for measuring PON1 activities and 1-hexadecyl-2-[3H]acetyl-glycero-3-phosphocholine for platelet-activating factor acetylhydrolase (PAF-AH) activity. Double substrate method was used to assign phenotypes. Lipid, lipoprotein, apolipoprotein, and lipoprotein particles were determined by standardized methods.


RESULTS
Both PON1 activities were significantly reduced in patients with low HDL-cholesterol levels. This reduction could be selectively attributed to the hypertriglyceridemic subgroup. PAF-AH activity was not different between hypoalphalipoproteinemic patients and controls. PON1 activities correlated positively and significantly with HDL-cholesterol, HDL2-cholesterol, HDL3-cholesterol, HDL-phospholipids, apo A-I, apo A-II, and LpA-I:A-II. PAF-AH correlated positively and significantly with total and low density lipoprotein-cholesterol.


CONCLUSIONS
Data from this study would suggest that in hypoalphalipoproteinemic syndrome, particularly when associated with hypertriglyceridemia, there is impairment in enzymatic antioxidant activity exclusively related with HDL.
Brites
Fernando Daniel
FD
Laboratorio de Lípidos y Lipoproteínas, Departamento de Bioquímica Clínica, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina. fbrites@dbc.ffyb.uba.ar
Verona
Julián
J
Schreier
Laura Ester
LE
Fruchart
Jean-Charles
JC
Castro
Graciela Rosa
GR
Wikinski
Regina Luisa
RL
D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000502:physiology*; D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000494:pharmacology; D043303:Aryldialkylphosphatase / Q000502:physiology*; D008076:Cholesterol, HDL / Q000378:metabolism*; D008078:Cholesterol, LDL / Q000378:metabolism; D006801:Humans; D015228:Hypertriglyceridemia / Q000473:pathology*; D050356:Lipid Metabolism; D008074:Lipoproteins / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D013997:Time Factors
D000975:Antioxidants; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008074:Lipoproteins; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D043303:Aryldialkylphosphatase