Noppawan Phumala MoralesChalermkhwan CherlermchoungSuthat FucharoenUdom ChantharaksriMahidol UniversityThe Institute of Science and Technology for Research and Development, Mahidol University2018-08-242018-08-242007-07-01Clinical Chemistry and Laboratory Medicine. Vol.45, No.7 (2007), 884-88914374331143466212-s2.0-34447263737https://repository.li.mahidol.ac.th/handle/20.500.14594/24171Background: Iron-induced oxidative stress may be implicated in the alteration of the lipoprotein-associated antioxidant enzymes paraoxonase 1 (PON1) and platelet-activating factor acetylhydrolase (PAF-AH), leading to atherosclerosis-related vascular complication in patients with β-thalassemia hemoglobin E (β-thal/Hb E). Methods: Plasma and lipoprotein enzyme activities of PON1 and PAF-AH were studied in 13 mild to moderate and 15 severe cases of β-thal/Hb E in comparison with 15 normal subjects. Results: PON1 activity was significantly reduced in association with oxidative stress in the patients. There were significant correlations between high-density lipoprotein (HDL)-PON1 activity and oxidative stress markers, including plasma levels of α-tocopherol (r=0.694 p<0.001) and the ratio of cholesteryl linoleate to cholesteryl oleate (CL/CO, r=0.662, p<0.001) in HDL. On the other hand, PAF-AH activity was markedly increased in patients by approximately two-fold and three- to four-fold in plasma and lipoproteins, respectively. Significant correlations of low-density lipoprotein (LDL) and HDL-PAF-AH activity with plasma iron, α-tocopherol and the CL/CO ratio were also demonstrated. Conclusions: We suggest that impairment of PON1 activity may be directly caused by oxidative damage, while increased PAF-AH activity possibly results from oxidative stress-induced inflammatory response in β-thal/Hb E patients. © 2007 by Walter de Gruyter.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyMedicineArticleSCOPUS10.1515/CCLM.2007.145