Elsevier

Environment International

Volume 121, Part 2, December 2018, Pages 1179-1184
Environment International

Oxidative damage in patients with benign prostatic hyperplasia and prostate cancer co-exposed to phthalates and to trace elements

https://doi.org/10.1016/j.envint.2018.10.034Get rights and content
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open access

Highlights

  • Trace elements and phthalate were analyzed in 60 subjects.

  • The most abundant metals were Hg in prostate cancer.

  • The most abundant metals were Cd, Cu and Ni in BPH.

  • Exposure to trace metals is more significant than is exposure to phthalates.

  • Exposure to phthalates and the pathogenesis of PCa and BPH are warranted.

Abstract

Evidence indicates that prostates exposed to environmental endocrine disruptors and trace metals will cause adverse health outcomes. We assessed the association between urinary phthalate metabolites and serum trace metal levels, and oxidative damage in benign prostatic hyperplasia (BPH) patients, prostate cancer (PCa) patients, and healthy controls. Levels of cadmium (Cd), nickel (Ni), and copper (Cu) were significantly higher in BPH patients than in controls, and mercury (Hg) was highest in PCa patients. An Hg level >1 μg/L posed a significant risk (OR: 42.86, 95% CI: 1.092–1684) for PCa, but a zinc (Zn) level >1 μg/L was marginally negative (OR: 0.979, 95% CI: 0.957–1.002). We also found strong associations between PCa and mono-isononyl phthalate (MiNP), and between BPH and mono-isodecyl phthalate (MiDP), malonyldialdehyde (MDA) were significantly higher in PCa and BPH patients than in controls; 8‑hydroxydeoxyguanosine (8‑OH‑dG) and DNA strand breakage were highest in BPH patients and lowest in controls. When the prostate was simultaneously co-exposed to phthalates and trace metals, phthalates had a less significant effect on PCa and BPH. Thus, we hypothesize that, for patients with prostate disease, exposure to trace metals is more significant than is exposure to phthalates.

Keywords

Metal
Phthalate
Prostatic cancer
Benign prostatic hyperplasia

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1

Equal contribution as first author.