[Single passive smoking exposure induces no measurable oxidation of low density lipoproteins].
Oxidation of low-density lipoproteins (LDL) is well known to increase the atherogenic risk. Active smoking has been claimed to be associated with a significant oxidant stress determined by enhanced LDL oxidation and isoprostane formation. We assessed the susceptibility of LDL to oxidation in 9 healthy non-smokers and 7 smokers before and after three and five hours' exposure to passive smoking. Baseline values for the lag time, diene formation, malondialdehyde and isoprostanes differed in part significantly. In contrast to the data on active smoking, passive exposure to cigarette smoke did not significantly affect any of these parameters, nor diene formation and electrophoretic mobility in smokers and non-smokers alike. These results indicate that a single exposure to passive smoking does not induce relevant oxidation of LDL in men.
Oguogho
A
A
Wilhelm-Auerswald Atheroskleroseforschungsgruppe und Universitätsklinik für Nuklearmedizin, Wien.
Kritz
H
H
Sinzinger
H
H
D000328:Adult; D001161:Arteriosclerosis / Q000097:blood*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D028441:F2-Isoprostanes; D005260:Female; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D010084:Oxidation-Reduction; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects* / Q000097:blood; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
D028441:F2-Isoprostanes; D008077:Lipoproteins, LDL; D014028:Tobacco Smoke Pollution; C075750:8-epi-prostaglandin F2alpha; D008315:Malondialdehyde; D015237:Dinoprost