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jeudi 12 juin 2014

Smoking deteriorates lipoprotein profile


Dysfunctional Lipoproteins from Young Smokers Exacerbate Cellular Senescence and Atherogenesis with Smaller Particle Size and Severe Oxidation and Glycation

  1. Kyung-Hyun Cho*,§,1

  1. *School of Biotechnology, Yeungnam University, Gyeongsan, 712-749, Republic of Korea
  2. Cardiovascular Division, Internal Medicine, Yeungnam University Medical Center, Daegu, 705-717, South Korea
  3. Research Institute of Protein Sensor, Yeungnam University, Gyeongsan, 712-749, Republic of Korea
  4. §BK21plus Program Serum Biomedical Research and Education Team, Yeungnam University, Gyeongsan, 712-749, Republic of Korea



Until now, there has been limited information on the effects of smoking on atherogenesis and senescence in the context of lipoprotein parameters, particularly in young smokers who have smoked fewer than 10 cigarettes per day for 3 years. In this study, lipoprotein profiles and functions were compared between smoker (n = 21) and control groups (n = 20). In the smoking group, ferric ion reduction abilities of serum and high-density lipoprotein (HDL) fractions were significantly reduced, and low-density lipoprotein (LDL) was severely oxidized. All lipoprotein particles from the smoker group showed higher advanced glycated end products with more triglyceride (TG) content compared to the control group. Lipoproteins from smokers showed faster agarose gel electromobility as well as greater smear band intensity in SDS-PAGE due to oxidation and glycation. LDL from smokers was more sensitive to oxidation and promoted foam cell forma-tion in macrophages. Gel filtration column chromatography revealed that the protein and cholesterol peaks of VLDL and LDL were elevated in the smoker group, whereas those of HDL were reduced. Human dermal fibroblast cells from the smoker group showed severe senescence following treatment with HDL2 and HDL3. Although HDL from young smokers showed impaired antioxidant ability, smaller particle size, and increased TG content, cholesteryl ester transfer protein activities were greatly enhanced in the serum and HDL fractions of the smoker group.In conclusion, smoking can cause production of dysfunctional lipoproteins having a smaller particle sizethat exacerbate senescence and atherogenic progress due to oxidation and glycation.


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