Oocyte exposure to low levels of triclosan has a significant impact on subsequent embryo physiology.
Triclosan (TCS) is an anti-microbial 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 nM and 10 nM) during in vitrao 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 also observed; specifically, O2 consumption coupled to ATP production was significantly decreased in COCs after acute exposure of 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 (12.22{+/-}% vs 29.11{+/-}% n=5; p=0.02) 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 mitochondria function, altered steroidogenesis and disrupted metabolic activity.