# Oocyte Exposure to Low Levels of Triclosan Has a Significant Impact on Subsequent Embryo Physiology

## TL;DR

Exposure of oocytes to low levels of triclosan during maturation leads to impaired embryo development and metabolism.

## Contribution

First evidence that triclosan exposure during oocyte maturation affects subsequent embryo physiology.

## Key findings

- Exposure to 1 nM triclosan increased progesterone release from bovine oocytes.
- Triclosan exposure caused mitochondrial dysfunction and altered pyruvate metabolism in COCs.
- Fewer TCS-exposed oocytes developed to blastocysts with impaired metabolic activity.

## Abstract

Triclosan (TCS) is an antimicrobial agent in a wide range of health care products. It has been found in various human bodily fluids and is a potential reproductive toxicant. However, the effect of TCS on early embryo development in mammalian species is limited. We therefore asked whether exposure to TCS affects mammalian cumulus–oocyte complexes (COCs), and if so, whether the effects persist into the early embryo. COCs, isolated from abattoir-derived bovine ovaries, were exposed to two environmentally relevant doses of TCS (1 and 10 nM) during in vitro maturation. When exposed to 1 nM TCS during in vitro maturation, progesterone release from bovine oocytes was elevated. Furthermore, altered pyruvate metabolism and mitochondrial dysfunction were also observed; specifically, O2 consumption coupled to ATP production was significantly decreased in COCs after acute exposure to TCS prior to maturation, whereas proton leak from the respiratory chain was increased. Subsequently, TCS-exposed COCs were fertilised. Fewer oocytes were able to develop to blastocyst when exposed to 1 nM TCS during maturation compared to the Control group, and those that did reach the blastocyst displayed impaired glycolytic and amino acid metabolic activity. These findings indicate for the first time that oocytes exposed to TCS during the final stages of maturation give rise to embryos with impaired mitochondrial function, altered steroidogenesis, and disrupted metabolic activity.