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T-2 toxin downregulates LHCGR expression, steroidogenesis, and cAMP level in human cumulus granulosa cells

Kristina Pogrmic-Majkic1, Dragana Samardzija Nenadov1, Bojana Stanic2

  • 1University of Novi Sad, Faculty of Sciences, Department of Biology and Ecology, Novi Sad, Serbia.

Environmental Toxicology
|April 6, 2019
PubMed

Insights

Environmentally relevant T-2 toxin impairs human granulosa cell function, reducing fertility. It likely acts by activating phosphodiesterase (PDE), disrupting hormone signaling crucial for ovulation.

Area of Science:

  • Reproductive Toxicology
  • Endocrinology
  • Cellular Signaling

Background:

  • T-2 toxin is a prevalent mycotoxin with potential adverse effects on reproductive health.
  • Human ovarian granulosa cells are critical for follicular development and ovulation.
  • Understanding T-2 toxin's impact on these cells is vital for assessing female fertility risks.

Purpose of the Study:

  • To investigate the effects of environmentally relevant T-2 toxin doses on human ovarian granulosa cell function.
  • To elucidate the underlying mechanism of T-2 toxin's action in these cells.

Main Methods:

  • Exposure of human cumulus granulosa cells to T-2 toxin under follicle-stimulating hormone (FSH) stimulation.
  • Quantification of key gene mRNA expression (LHCGR, CYP19A1, STAR, ovulatory genes).
  • Measurement of steroid production (estradiol, progesterone) and cyclic adenosine monophosphate (cAMP) levels.
  • Assessment of T-2 toxin's effects with and without phosphodiesterase (PDE) inhibitors and 8-bromoadenosine 3'5'-cyclic monophosphate (8-Br-cAMP).

Main Results:

  • T-2 toxin significantly reduced luteinizing hormone/choriogonadotropin receptor (LHCGR) mRNA expression.
  • It attenuated FSH-stimulated steroidogenesis (estradiol, progesterone) and ovulatory gene expression.
  • T-2 toxin decreased FSH-stimulated cAMP production, an effect partially reversed by PDE inhibition.

Conclusions:

  • Environmentally relevant T-2 toxin doses impair human granulosa cell steroidogenesis and ovulatory potential.
  • The mechanism involves T-2 toxin-induced activation of phosphodiesterase (PDE), leading to reduced cAMP signaling.
  • These findings highlight a significant risk posed by T-2 toxin to female fertility.
Keywords:
LHCGRPDET-2 toxincAMPhuman cumulus granulosa cellsovulatory processessteroidogenesis

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