Bisphenol S reduces locomotor performance and modifies muscle protein levels but not mitochondrial bioenergetics in adult zebrafish

Abstract

Human activity has now introduced novel chemicals into most aquatic ecosystems. Endocrine-disrupting compounds originating from plastic pollution and manufacture can have pronounced biological effects by disrupting hormone-mediated processes. Bisphenol A (BPA) is one of the most commonly produced endocrine-disrupting compounds, which interferes with signalling by a broad range of hormones. In recognition of its potentially harmful effects, BPA is being replaced by substitutes such as bisphenol S (BPS). However, toxicological studies revealed that BPS too can bind to hormone receptors and disrupt signalling, particularly of thyroid hormone. The aim of this study was to test whether BPS exposure impacts locomotor performance and muscle function in zebrafish (Danio rerio). Locomotor performance depends on thyroid hormone signalling, and it is closely related to fitness so that its disruption can have negative ecological and evolutionary consequences. BPS exposure of 15 μg l−1 [∼60 nM] and 30 μg l−1 (but not 60 μg l−1) decreased sustained swimming performance (Ucrit), but not sprint speed. In a fully factorial design, we show that living in flowing water increased Ucrit compared to a still water control, and that BPS reduced Ucrit under both conditions but did not eliminate the training effect. In a second factorial experiment, we show that BPS did not affect mitochondrial bioenergetics in skeletal muscle (state 3 and 4 rates, respiratory control ratios, ROS production), but that induced hypothyroidism decreased state 3 and 4 rates of respiration. However, both hypothyroidism and BPS exposure decreased activity of AMP-activated protein kinase (pAMPK:total AMPK) but increased protein levels of myocyte enhancer factor 2, and slow and fast myosin heavy chains. Our data indicate that BPS is not a safe alternative for BPA and that exposure to BPS can have ecological consequences, which are likely to be at least partly mediated via thyroid hormone disruption.