Elevated plasma 8-iso-prostaglandin F2α levels in human smokers originate primarily from enzymatic instead of non-enzymatic lipid peroxidation

Publication date: 1 February 2018
Source:Free Radical Biology and Medicine, Volume 115
Author(s): Thomas J. van 't Erve, Fred B. Lih, Maria B. Kadiiska, Leesa J. Deterding, Ronald P. Mason
It is widely accepted that free radicals in tobacco smoke lead to oxidative stress and generate the popular lipid peroxidation biomarker 8-iso-prostaglandin F2α (8-iso-PGF2α). However, 8-iso-PGF2α 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-PGF2α in tobacco smokers.The goal of this study is to quantify the distribution of chemical- and PGHS-dependent 8-iso-PGF2α 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-PGF2α/prostaglandin F2α (PGF2α) ratio.When comparing smokers (n = 28) against non-smokers (n = 30), there was a statistically significant increase in the 8-iso-PGF2α concentration. The source of this increased 8-iso-PGF2α was primarily from PGHS. When stratifying for gender, the increase in 8-iso-PGF2α in male smokers (n = 9) was primarily from PGHS. Interestingly, female smokers on hormonal contraceptives had increased 8-iso-PGF2α in both pathways, whereas those not on hormonal contraceptives did not have increased 8-iso-PGF2α.In conclusion, increased plasma 8-iso-PGF2α 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.

Graphical abstract

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