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Estrogenic effect of procymidone through activation of MAPK in MCF-7 breast carcinoma cell line

Sonia Radice1, Enzo Chiesara, Silvia Frigerio

  • 1Department of Pharmacology, Chemotherapy and Medical Toxicology E. Trabucchi, University of Milan, Via Vanvitelli 32, 20129 Milan, Italy. sonia.radice@unimi.it

Life Sciences
|November 29, 2005
PubMed

Insights

The fungicide procymidone causes estrogenic effects in human cells indirectly by activating mitogen-activated protein kinase (MAPK) through reactive oxygen species (ROS). This endocrine-disrupting chemical

Area of Science:

  • Endocrinology
  • Environmental Toxicology
  • Cell Biology

Background:

  • Fungicides like procymidone can disrupt endocrine systems.
  • Procymidone has been detected in human tissues, raising concerns about its safety.
  • Previous studies indicated procymidone's estrogenic activity in fish models.

Purpose of the Study:

  • To investigate procymidone's endocrine-disrupting potential in human MCF-7 cells.
  • To elucidate the mechanism behind procymidone's estrogenic action.
  • To determine if procymidone interacts with estrogen receptors (ER) or other signaling pathways.

Main Methods:

  • MCF-7 cells were treated with procymidone (100 microM).
  • Cell growth and pS2 protein levels were measured.
  • Estrogen receptor (ER) involvement was assessed using antiestrogen ICI 182780.
  • Mitogen-activated protein kinase (MAPK) and c-Neu receptor pathways were investigated.
  • Reactive oxygen species (ROS) production was evaluated using ROS scavengers like alpha-tocopherol (alpha-T).

Main Results:

  • Procymidone stimulated MCF-7 cell growth and increased pS2 levels.
  • Procymidone's effects were inhibited by ICI 182780, suggesting indirect ER involvement.
  • Procymidone did not activate the c-Neu receptor pathway.
  • Procymidone induced MAPK (Erk1/2) activation, which was blocked by PD 98059.
  • Procymidone induced ROS production, which was mitigated by alpha-T, indicating ROS mediate MAPK activation.

Conclusions:

  • Procymidone exhibits estrogenic activity in human cells through an indirect mechanism.
  • The pathway involves ROS generation leading to MAPK activation, which then influences ER signaling.
  • Procymidone does not directly bind to the ER or activate the c-Neu receptor.
  • These findings highlight procymidone as a potential endocrine disruptor with implications for human health.

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