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Background <p>Endocrine-disrupting chemicals (EDCs) are environmental pollutants capable of interfering with hormonal regulation and affecting the homeostasis of hormone-dependent organs such as the prostate. Increasing evidence links exposure to EDCs with prostate inflammation, oxidative stress, and carcinogenesis. These compounds, found in pesticides, plastics, surfactants, and heavy metals, act through diverse molecular pathways that disrupt endocrine, immune, and metabolic functions.</p> Purpose of Review <p>From this perspective, the present review aims to synthesize current findings on the effects of EDCs on inflammation and oxidative stress in the prostate, highlighting experimental evidence from in vitro and in vivo models and discussing the main molecular mechanisms involved.&#xa0;</p> Recent Findings <p>Recent studies have strengthened the evidence that EDCs play a critical role in prostate pathophysiology by integrating inflammatory, oxidative, and epigenetic mechanisms. Advances in molecular biology have revealed that EDC exposure can modulate key signaling pathways, including NF-κB, TLR4, and TNF-α, leading to sustained inflammatory responses and disruption of redox homeostasis in prostatic cells.</p> Results <p>Experimental studies demonstrate that EDCs such as bisphenol A, phthalates, nonylphenol, cadmium, arsenic, and vinclozolin induce inflammatory and oxidative alterations in prostate tissue. These effects include activation of pro-inflammatory signaling pathways, increased expression of cytokines, and upregulation of oxidative stress markers. Concurrently, these compounds impair antioxidant defense systems by modulating enzymes such as catalase, superoxide dismutase, and glutathione reductase. Chronic exposure promotes cellular proliferation, epithelial dysplasia, apoptotic resistance, and epigenetic modifications, contributing to prostate pathogenesis and tumorigenesis.</p> Conclusion <p>EDCs exert profound effects on prostatic physiology by disrupting endocrine balance, promoting chronic inflammation, and inducing oxidative stress. The interplay between these processes establishes a microenvironment favorable to cellular transformation and tumor progression.</p>

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The effects of endocrine disrupting chemicals on inflammation and oxidative stress in the prostate: an overview in different experimental models

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月29日

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  • Ana Clara Pacheco de Santana,
  • Eleonora Pizzo Liboni,
  • Vinícius Luis Rocha da Silva Maria,
  • Sergio Pereira,
  • Cristiane Figueiredo Pinho

摘要

Background

Endocrine-disrupting chemicals (EDCs) are environmental pollutants capable of interfering with hormonal regulation and affecting the homeostasis of hormone-dependent organs such as the prostate. Increasing evidence links exposure to EDCs with prostate inflammation, oxidative stress, and carcinogenesis. These compounds, found in pesticides, plastics, surfactants, and heavy metals, act through diverse molecular pathways that disrupt endocrine, immune, and metabolic functions.

Purpose of Review

From this perspective, the present review aims to synthesize current findings on the effects of EDCs on inflammation and oxidative stress in the prostate, highlighting experimental evidence from in vitro and in vivo models and discussing the main molecular mechanisms involved. 

Recent Findings

Recent studies have strengthened the evidence that EDCs play a critical role in prostate pathophysiology by integrating inflammatory, oxidative, and epigenetic mechanisms. Advances in molecular biology have revealed that EDC exposure can modulate key signaling pathways, including NF-κB, TLR4, and TNF-α, leading to sustained inflammatory responses and disruption of redox homeostasis in prostatic cells.

Results

Experimental studies demonstrate that EDCs such as bisphenol A, phthalates, nonylphenol, cadmium, arsenic, and vinclozolin induce inflammatory and oxidative alterations in prostate tissue. These effects include activation of pro-inflammatory signaling pathways, increased expression of cytokines, and upregulation of oxidative stress markers. Concurrently, these compounds impair antioxidant defense systems by modulating enzymes such as catalase, superoxide dismutase, and glutathione reductase. Chronic exposure promotes cellular proliferation, epithelial dysplasia, apoptotic resistance, and epigenetic modifications, contributing to prostate pathogenesis and tumorigenesis.

Conclusion

EDCs exert profound effects on prostatic physiology by disrupting endocrine balance, promoting chronic inflammation, and inducing oxidative stress. The interplay between these processes establishes a microenvironment favorable to cellular transformation and tumor progression.