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Free Radic Biol Med. 2018 Feb 1;115:105-112. doi: 10.1016/j.freeradbiomed.2017.11.008. Epub 2017 Nov 21.

Elevated plasma 8-iso-prostaglandin F levels in human smokers originate primarily from enzymatic instead of non-enzymatic lipid peroxidation.

Author information

1
Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, 27709 NC, USA. Electronic address: thomas.vanterve@nih.gov.
2
Epigenetic and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, 27709 NC, USA.
3
Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, 27709 NC, USA.

Abstract

It is widely accepted that free radicals in tobacco smoke lead to oxidative stress and generate the popular lipid peroxidation biomarker 8-iso-prostaglandin F (8-iso-PGF). However, 8-iso-PGF can simultaneously be produced in vivo by the prostaglandin-endoperoxide synthases (PGHS) induced by inflammation. This inflammation-dependent mechanism has never been considered as a source of elevated 8-iso-PGF in tobacco smokers. The goal of this study is to quantify the distribution of chemical- and PGHS-dependent 8-iso-PGF formation in the plasma of tobacco smokers and non-smokers. The influences of gender and hormonal contraceptive use were accounted for. The distribution was determined by measuring the 8-iso-PGF/prostaglandin F (PGF) ratio. When comparing smokers (n = 28) against non-smokers (n = 30), there was a statistically significant increase in the 8-iso-PGF concentration. The source of this increased 8-iso-PGF was primarily from PGHS. When stratifying for gender, the increase in 8-iso-PGF in male smokers (n = 9) was primarily from PGHS. Interestingly, female smokers on hormonal contraceptives had increased 8-iso-PGF in both pathways, whereas those not on hormonal contraceptives did not have increased 8-iso-PGF. In conclusion, increased plasma 8-iso-PGF in tobacco smokers has complex origins, with PGHS-dependent formation as the primary source. Accounting for both pathways provides a definitive measurement of both oxidative stress and inflammation.

KEYWORDS:

8-iso-PGF(2α) / PGF(2α) ratio; Biomarkers; F(2)-isoprostanes; Inflammation; Lipid peroxidation; Oxidative stress

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