Parental whole life-cycle exposure to tris (2-chloroethyl) phosphate (TCEP) disrupts embryonic development and thyroid system in zebrafish offspring

Abstract

Tris (2-chloroethyl) phosphate (TCEP), an emerging environmental pollutant, has been frequently detected in natural waters. The objective of this study was to investigate possible parental transfer of TCEP and transgenerational effects on the early development and thyroid hormone homeostasis in F1 larvae following parental whole life-cycle exposure to TCEP. To this end, zebrafish (Danio rerio) embryos were exposed to environmentally relevant concentrations (0.8, 4, 20 and 100 μg/L) of TCEP for 120 days until sexual maturation. Parental exposure to TCEP resulted in significant levels of TCEP, developmental toxicity including decreased survival and final hatching rates, accelerated heart rate and elevated malformation rate, as well as induction of oxidative stress and cell apoptosis in F1 offspring. In F1 eggs, declined thyroxin (T4) levels were observed, consistent with those in plasma of F0 adult females, indicating the maternal transfer of thyroid endocrine disruption to the offspring. In addition, mRNA levels of several genes along the hypothalamic-pituitary-thyroid (HPT) axis were significantly modified in F1 larvae, which could be linked to transgenerational developmental toxicity and thyroid hormone disruption. For the first time, we revealed that the parental exposure to environmentally relevant levels of TCEP could cause developmental toxicity and thyroid endocrine disruption in subsequent unexposed generation.

Keywords

• Organophosphate ester
• Zebrafish
• Developmental toxicity
• Oxidative stress
• Cell apoptosis
• Thyroid endocrine disruption