Publication: The reduction of cholesteryl linoleate in lipoproteins: An index of clinical severity in β-thalassemia/Hb E
Issued Date
2006-05-01
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ISSN
14346621
14346621
14346621
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2-s2.0-33646692249
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Mahidol University
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SCOPUS
Bibliographic Citation
Clinical Chemistry and Laboratory Medicine. Vol.44, No.5 (2006), 574-581
Suggested Citation
Rataya Luechapudiporn, Noppawan Phumala Morales, Suthat Fucharoen, Udom Chantharaksri The reduction of cholesteryl linoleate in lipoproteins: An index of clinical severity in β-thalassemia/Hb E. Clinical Chemistry and Laboratory Medicine. Vol.44, No.5 (2006), 574-581. doi:10.1515/CCLM.2006.093 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/23047
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Title
The reduction of cholesteryl linoleate in lipoproteins: An index of clinical severity in β-thalassemia/Hb E
Abstract
Background: Oxidative modification of lipoproteins has been reported in β-thalassemia and has been suggested to relate to atherogenesis-risk. This study focused on the change in cholesteryl esters in plasma lipoproteins under oxidative stress resulting from iron overload in β-thalassemia/hemoglobin E (β-thal/Hb E) patients. Methods: Markers of oxidative damage and cholesteryl esters (CEs) were measured in plasma and lipoproteins from 30 β-thal/Hb E patients and compared to those from 10 healthy volunteers. CEs in plasma, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) were separated and identified using HPLC. Results: β-Thal/Hb E patients presented iron overload, a precipitous decrease in α-tocopherol and increased lipid peroxidation (thiobarbituric acid-reactive substances; TBARs) in both plasma and lipoproteins. Cholesteryl linoleate, the most abundant CE in lipoproteins, showed a reduction of 70% in LDL, while other CEs showed a lower reduction (50%). An inverse relationship between the cholesteryl linoleate/cholesteryl oleate ratio (CL/CO) and the degree of clinical severity suggested that the CL/CO ratio is an index of damaged lipoproteins and could be used as a pathologic marker of underlying iron overload. Good correlation of non-transferrin-bound iron (NTBI) and TBARs (r = 0.8, p < 0.01) in LDL strongly supported the contention that iron overload is responsible for initiating the lipid peroxidation in β-thal/Hb E. Conclusions: This study suggests that cholesteryl linoleate is the primary target of oxidative modification induced by NTBI in β-thal/Hb E patients and that reduction in cholesteryl linoleate in lipoproteins could be used as a severity index for β-thal/Hb E. © 2006 by Walter de Gruyter.