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Oxidative stress promotes benign prostatic hyperplasia.

Paz Vital1, Patricia Castro1, Michael Ittmann1

  • 1Department of Pathology and Immunology, Baylor College of Medicine and Michael E. DeBakey Department of Veterans Affairs Medical Center, Houston, Texas.

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|September 30, 2015
PubMed
Summary
This summary is machine-generated.

Oxidative stress and DNA damage, marked by 8-OH deoxyguanosine (8-OH dG), are significantly elevated in benign prostatic hyperplasia (BPH) tissues. These findings suggest a causal role for oxidative stress in BPH development.

Keywords:
Nox4benign prostatic hyperplasiaoxidative DNA damageoxidative stresstransgenic

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Area of Science:

  • Urology
  • Molecular Biology
  • Pathology

Background:

  • Benign prostatic hyperplasia (BPH) involves prostate tissue growth, causing urinary obstruction and morbidity in aging men.
  • Elevated plasma oxidative stress markers are observed in BPH patients, but a causal link remains unclear.

Purpose of the Study:

  • To investigate the role of oxidative stress and DNA damage in the pathogenesis of benign prostatic hyperplasia.
  • To determine if 8-OH deoxyguanosine (8-OH dG) levels correlate with BPH severity.

Main Methods:

  • Quantified 8-OH dG, an oxidative stress marker, in normal and BPH prostate tissues using ELISA and immunohistochemistry.
  • Generated and analyzed transgenic mice with prostate-specific Nox4 expression to model oxidative stress.

Main Results:

  • Human BPH tissues showed significantly higher 8-OH dG levels, correlated with prostate weight.
  • Increased epithelial 8-OH dG staining was observed in BPH tissues.
  • Transgenic mice exhibited increased prostate oxidative DNA damage, weight, epithelial proliferation, and fibrosis.

Conclusions:

  • Oxidative stress and associated DNA damage are key contributors to the pathogenesis of benign prostatic hyperplasia.
  • The findings support a causal role for oxidative stress in BPH development.