Summary
The possible influence of smoking on the low-density lipoprotein (LDL) and its biological activity was investigated. Plasma LDL was prepared from healthy male smokers and nonsmokers, and oxidized with Cu (11) as prooxidant. Oxidized LDL from smokers generated significantly more lipidperoxidation products, so-called thiobarbituric acid reactive substances (TBARS), when compared to oxidized nonsmoker LDL. Analysis of vitamin E levels in LDL obtained from both smokers and nonsmokers revealed that the vitamin E content of smoker LDL was significantly less than that of nonsmoker LDL. The amounts of cholesteryl esters formed in cultured P388. D.1 macrophages were greater in the presence of smoker LDL than with nonsmoker LDL. The data suggest that some of the proatherogenic effects of smoking may be related to oxidative modification of LDL and alteration of its biological activity.
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Abbreviations
- CE:
-
cholesterol ester
- FC:
-
free cholesterol
- FCS:
-
fetal calf serum
- HPLC:
-
high performance liquid chromatography
- LDL:
-
low-density lipoprotein
- MDA:
-
malondialdehyde
- PUFA:
-
polyunsaturated fatty acid
- SD:
-
standard deviation
- TBA:
-
thiobarbituric acid
- TBARS:
-
thiobarbituric acid reactive substances
- TLC:
-
thin-layer chromatography
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Scheffler, E., Wiest, E., Woehrle, J. et al. Smoking influences the atherogenic potential of low-density lipoprotein. Clin Investig 70, 263–268 (1992). https://doi.org/10.1007/BF00184660
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DOI: https://doi.org/10.1007/BF00184660