Iodoacetic acid inhibits follicle growth and alters expression of genes that regulate apoptosis, the cell cycle, estrogen receptors, and ovarian steroidogenesis in mouse ovarian follicles

Andressa Gonsioroski, Daryl D. Meling, Liying Gao, Michael Jacob Plewa, Jodi A. Flaws

Research output: Contribution to journalArticlepeer-review

Abstract

The reaction between disinfectants and organic matter or inorganic matter in source water generates disinfection by-products (DBPs) such as iodoacetic acid (IAA). DBPs are associated with health effects such as bladder cancer and adverse reproductive outcomes, but the effects of IAA on the ovary are not well known. This study determined whether IAA exposure affects ovarian follicle growth, steroidogenesis, and expression of apoptotic factors, cell cycle regulators, estrogen receptors, and steroidogenic factors in vitro. IAA exposure significantly decreased follicle growth, expression of cell cycle stimulators, and the proliferation marker Ki67. In contrast, IAA increased expression of the cell cycle inhibitor Cdkn1a. Moreover, IAA exposure increased expression of pro-apoptotic factors, whereas it decreased expression of anti-apoptotic factors. IAA exposure also altered expression of steroidogenic factors and estrogen receptors, disrupting steroidogenesis. These data demonstrate that IAA exposure inhibits follicle growth, decreases cell proliferation, and alters steroidogenesis in mouse ovarian follicles in vitro.

Original languageEnglish (US)
Pages (from-to)101-108
Number of pages8
JournalReproductive Toxicology
Volume91
DOIs
StatePublished - Jan 2020

Keywords

  • Disinfection by-products
  • Folliculogenesis
  • Iodoacetic acid
  • Ovary
  • Steroidogenesis

ASJC Scopus subject areas

  • Toxicology

Fingerprint

Dive into the research topics of 'Iodoacetic acid inhibits follicle growth and alters expression of genes that regulate apoptosis, the cell cycle, estrogen receptors, and ovarian steroidogenesis in mouse ovarian follicles'. Together they form a unique fingerprint.

Cite this