Abstract
Triclosan (TCS) is one of the most common endocrine-disrupting chemicals (EDCs) present in household and personal wash products. Recently, concerns have been raised about the association between abnormal behavior in children and exposure to EDC during gestation. We hypothesized that exposure to TCS during gestation could affect brain development. Cortical neurons of mice were exposed in vitro to TCS. In addition, we examined in vivo whether maternal TCS administration can affect neurobehavioral development in the offspring generation. We determined that TCS can impair dendrite and axon growth by reducing average length and numbers of axons and dendrites. Additionally, TCS inhibited the proliferation of and promoted apoptosis in neuronal progenitor cells. Detailed behavioral analyses showed impaired acquisition of spatial learning and reference memory in offspring derived from dams exposed to TCS. The TCS-treated groups also showed cognition dysfunction and impairments in sociability and social novelty preference. Furthermore, TCS-treated groups exhibited increased anxiety-like behavior, but there was no significant change in depression-like behaviors. In addition, TCS-treated groups exhibited deficits in nesting behavior. Taken together, our results indicate that perinatal exposure to TCS induces neurodevelopment disorder, resulting in abnormal social behaviors, cognitive impairment, and deficits in spatial learning and memory in offspring.
Highlights
Triclosan (TCS) is widely used in consumer products as an antibacterial agent and is found in toothpaste, mouthwash, soap, deodorants, textiles, toys, and medical devices [1]
TCS at a high concentration can slightly delay the development of secondary motor neurons in zebrafish [17]. These findings show that TCS may induce adverse effects on the central nervous system (CNS) functions via apoptosis and oxidative stress [12]
We found that maternal exposure to TCS during pregnancy and lactation decreased mRNA levels of thyroid hormone-related genes such as thyroglobulin (Tg), thyroperoxidase (Tpo), sodium-iodide symporter (Nis), monocarboxylate transporter 8 (Mct8) and thyrotropin receptor (Tshr) in the thyroid gland at postnatal day (PND) 119 (Supplementary Figure S2)
Summary
Triclosan (TCS) is widely used in consumer products as an antibacterial agent and is found in toothpaste, mouthwash, soap, deodorants, textiles, toys, and medical devices [1]. In rats, disrupted fetal development and embryonic developmental delay can be caused by prenatal exposure to TCS [10]. Exposure to TCS during gestation may impair placental development and nutrient transfer, leading to decreases in fetal body weight by inducing hypothyroxinemia through a reduction in Akt-mTOR signaling [11]. TCS at a high concentration can slightly delay the development of secondary motor neurons in zebrafish [17]. These findings show that TCS may induce adverse effects on the central nervous system (CNS) functions via apoptosis and oxidative stress [12]. The effects of maternal TCS exposure as well as other EDCs on brain development and behavioral abilities in offspring remain insufficiently described
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