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Active smoking and a history of smoking are associated with enhanced prostaglandin F(2alpha), interleukin-6 and F(2)-isoprostane formation in elderly men
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition Research.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Biochemial structure and function.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition Research.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Clinical Nutrition Research.
2005 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 181, no 1, 201-207 p.Article in journal (Refereed) Published
Abstract [en]

The underlying mechanisms by which smoking induces cardiovascular diseases are largely unknown. The effect of smoking status on the cyclooxygenase (COX)-mediated inflammatory indicator prostaglandin F(2alpha) (PGF(2alpha)) has never been studied. Associations of cytokines and antioxidants and smoking status, have shown conflicting results. Urinary 15-keto-dihydro-PGF(2alpha) (a major metabolite of PGF(2alpha)), serum interleukin-6 (IL-6) and high sensitivity C-reactive protein (hsCRP), serum amyloid protein A (SAA), urinary 8-iso-PGF(2alpha) (an F(2)-isoprostane, indicator of oxidative stress), and serum alpha-tocopherol were quantified in a population-based sample (n = 642) of 77-year old men without diabetes. Fifty-five men were current smokers and 391 former smokers. Inflammatory indicators were increased in current smokers (15-keto-dihydro-PGF(2alpha), P < 0.001; IL-6, P = 0.01) than non-smokers. 8-iso-PGF(2alpha) was increased (P < 0.01) and alpha-tocopherol reduced (P < 0.001) in current smokers. Further, former smokers had increased formation of 15-keto-dihydro-PGF(2alpha), IL-6 and 8-iso-PGF(2alpha) compared non-smokers. This is the first study to show that smokers have increased PGF(2alpha) formation, thus enhanced COX-mediated inflammation, in addition to elevated levels of cytokines and isoprostanes. Subclinical COX- and cytokine-mediated inflammation and oxidative stress are ongoing processes not only in active smokers but also in former smokers which may contribute to the accelerated atherosclerosis associated with smoking.

Place, publisher, year, edition, pages
2005. Vol. 181, no 1, 201-207 p.
Keyword [en]
Aged, Aging/*metabolism, Antioxidants/metabolism, Biological Markers/blood/urine, C-Reactive Protein/metabolism, Cohort Studies, Cytokines/metabolism, Dinoprost/analogs & derivatives/*biosynthesis/urine, F2-Isoprostanes/*biosynthesis, Humans, Inflammation/etiology, Interleukin-6/*biosynthesis/blood, Longitudinal Studies, Male, Oxidative Stress, Prostaglandin-Endoperoxide Synthases/metabolism, Smoking/*adverse effects, Smoking Cessation, Time Factors, Tocopherols/blood
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-92656DOI: 10.1016/j.atherosclerosis.2004.11.026PubMedID: 15939073OAI: oai:DiVA.org:uu-92656DiVA: diva2:165817
Available from: 2005-03-10 Created: 2005-03-10 Last updated: 2013-09-05Bibliographically approved
In thesis
1. Prostaglandins and Isoprostanes in Relation to Risk Factors for Atherosclerosis: Role of Inflammation and Oxidative Stress
Open this publication in new window or tab >>Prostaglandins and Isoprostanes in Relation to Risk Factors for Atherosclerosis: Role of Inflammation and Oxidative Stress
2005 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Inflammation and oxidative stress may be involved in atherogenesis. This thesis describes clinical studies of prostaglandin F (PGF), an inflammatory mediator, and the isoprostane 8-iso-PGF, a reliable indicator of oxidative stress, and cytokine-related inflammatory mediators and indicators in healthy subjects and in a population-based cohort of Swedish men.

PGF and 8-iso-PGF formation in healthy subjects varied considerably between days with a mean intra-individual coefficient of variation of 41 % and 42 %, respectively. A morning urine sample reflected the basal level of 8-iso-PGF formation as accurately as a 24-hour urine collection, and represents a more practical alternative to the 24-hour urine collection in clinical studies. PGF formation (as measured by urinary 15-keto-dihydro-PGF) was increased in patients with type 2 diabetes and in smokers independent of other cardiovascular risk factors. These results indicated an on-going cyclooxygenase (COX)-mediated inflammatory reaction related to these conditions. Further, an increased formation of isoprostanes (as measured by urinary 8-iso-PGF) was found in patients with type 2 diabetes and in smokers, indicating a high level of oxidative stress in these men. The smokers had also increased levels of the cytokine interleukin-6, indicating an on-going cytokine-related inflammatory reaction. The inflammatory indicators C-reactive protein and serum amyloid A were related to overweight but not independently associated to type 2 diabetes. High levels of serum selenium in middle-aged men predicted reduced formation of PGF and 8-iso-PGF 27 years later.

In summary, low-grade, chronic COX-mediated and possibly cytokine-related inflammation, and oxidative stress, seem to be joint features of type 2 diabetes and smoking, two major risk factors of atherosclerosis, in elderly men. Inflammation and oxidative stress may represent a possible common pathogenetic link between established risk factors for atherosclerosis and atherogenesis.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2005. 82 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 9
Keyword
Public health, prostaglandin F2α, F2-isoprostane, interleukin-6, C-reactive protein, serum amyloid A, tocopherols, cardiovascular risk factors, variation, inflammation, oxidative stress, human, Folkhälsomedicin
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:uu:diva-4803 (URN)91-554-6156-5 (ISBN)
Public defence
2005-04-01, Auditorium Minus, Museum Gustavianum, Akademigatan 3, Uppsala, 09:15
Opponent
Supervisors
Available from: 2005-03-10 Created: 2005-03-10Bibliographically approved

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Helmersson, JohannaLarsson, AndersVessby, BengtBasu, Samar

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