Elevated plasma 8-iso-prostaglandin F2? levels in human smokers originate primarily from enzymatic instead of non-enzymatic lipid peroxidation.
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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 F2? (8-iso-PGF2?). However, 8-iso-PGF2? 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-PGF2? in tobacco smokers. The goal of this study is to quantify the distribution of chemical- and PGHS-dependent 8-iso-PGF2? 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-PGF2?/prostaglandin F2? (PGF2?) ratio. When comparing smokers (n = 28) against non-smokers (n = 30), there was a statistically significant increase in the 8-iso-PGF2? concentration. The source of this increased 8-iso-PGF2? was primarily from PGHS. When stratifying for gender, the increase in 8-iso-PGF2? in male smokers (n = 9) was primarily from PGHS. Interestingly, female smokers on hormonal contraceptives had increased 8-iso-PGF2? in both pathways, whereas those not on hormonal contraceptives did not have increased 8-iso-PGF2?. In conclusion, increased plasma 8-iso-PGF2? 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.
SUBMITTER: van 't Erve TJ
PROVIDER: S-EPMC5767525 | biostudies-literature | 2018 Feb
REPOSITORIES: biostudies-literature
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