Waterborne exposure to microcystin‐lr causes thyroid hormone metabolism disturbances in juvenile chinese rare minnow (Gobiocypris rarus)

Microcystin‐LR (MC‐LR) has the potential to disturb thyroid hormone (TH) homeostasis, but little is known of the underlying mechanisms of MC‐LR in fish. In the present study, juvenile Chinese rare minnows (Gobiocypris rarus) were exposed to various concentrations of MC‐LR (0, 50, 100, and 500 μg/L) for 7 d. The whole‐body content of THs, the histology of thyroid follicle epithelial cells, the activities of hepatic iodothyronine deiodinases (IDs), and the transcription of selected genes associated with TH synthesis, transport, and metabolism were analyzed. Following exposure to MC‐LR, whole‐body concentrations of both thyroxine (T4) and triiodothyronine (T3) were significantly decreased. The levels of mRNA for sodium/iodide symporter (NIS), transthyretin (TTR), thyroid hormone receptor (TR)‐α, ID2, and ID3 were significantly down‐regulated after exposure to 500 μg/L MC‐LR. A significant decrease in ID2 activity was also observed in the 500 μg/L MC‐LR exposure group. Moreover, the hypertrophy of thyroid follicle epithelial cells was observed upon exposure to MC‐LR. The results indicate that acute MC‐LR exposure has the potential to disturb the homeostasis of thyroid hormone metabolism, leading to a hypothyroidism state in the juvenile Chinese rare minnow. This article is protected by copyright. All rights reserved