3 research outputs found
Prenatal Nonylphenol and Bisphenol A Exposures and Inflammation Are Determinants of Oxidative/Nitrative Stress: A Taiwanese Cohort Study
Prenatal
exposure to nonylphenol (NP) and/or bisphenol A (BPA)
has been reported to be associated with adverse birth outcomes; however,
the underlying mechanisms remain unclear. The primary mechanism is
endocrine disruption of the binding affinity for the estrogen receptor,
but oxidative stress and inflammation might also play a contributory
role. We aimed to investigate urinary NP and BPA levels in relation
to biomarkers of oxidative/nitrative stress and inflammation and to
explore whether changes in oxidative/nitrative stress are a function
of prenatal exposure to NP/BPA and inflammation in 241 mother-fetus
pairs. Third-trimester urinary biomarkers of oxidative/nitrative stress
were simultaneously measured, including products of oxidatively and
nitratively damaged DNA (8-hydroxy-2′-deoxyguanosine (8-OHdG)
and 8-nitroguanine (8-NO<sub>2</sub>Gua)) as well as products of lipid
peroxidation (8-iso-prostaglandin F<sub>2α</sub> (8-isoPF<sub>2α</sub>) and 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA)).
The antioxidant glutathione peroxidase (GPx) and inflammation biomarkers,
including C-reactive protein (CRP) and a panel of cytokines (interleukin-6
(IL-6) and tumor necrosis factor-α (TNF-α)), were analyzed
in maternal and umbilical cord plasma samples. In adjusted models,
we observed significant positive associations between NP exposure
and 8-OHdG and 8-NO<sub>2</sub>Gua levels, between BPA and 8-isoPF<sub>2α</sub> levels, and between maternal CRP levels and HNE-MA
levels. Additionally, BPA and TNF-α levels in cord blood were
inversely associated with maternal and GPx levels in cord blood as
well as maternal TNF-α levels were inversely associated with
maternal GPx levels. These results support a role for exposure to
NP and BPA and possibly inflammation in increasing oxidative/nitrative
stress and decreasing antioxidant activity during pregnancy