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Nitrate is known to disrupt the thyroid hormone, which is essential for the metamorphosis of amphibians. However, few studies are focused on the effects of nitrate on the maternal thyroid hormone in early amphibian embryos. We aimed to determine the impact of nitrate on maternal thyroid hormone signaling pathway in Bufo gargarizans embryos. B. gargarizans embryos were exposed to different concentrations of nitrate-nitrogen (NO3-N) for 7 days. High concentration of NO3-N (50, 100, and 200 mg/L) could induce embryonic malformation and influence the development of embryos. In addition, maternal T4 and components of the thyroid hormone (TH) signaling pathway were detected by ELISA and RNA-seq, respectively. The expression levels of mRNA related to thyroid hormone and oxidative stress were affected in the early developing embryos in all NO3-N treatment groups. However, the T4 levels and the spatial expression patterns of type II iodothyronine deiodinase (D2), type III iodothyronine deiodinase (D3), thyroid hormone receptor α (TRα), and thyroid hormone receptor β (TRβ) mRNA were not changed by nitrate. In conclusion, the results of our study highlight the crucial role of the maternal thyroid hormone signaling pathway in normal embryonic development, and the adverse effects of nitrate on the expression levels of mRNA related to thyroid hormone signaling pathway and oxidative stress in B. gargarizans embryos.

Microcystin-LR (MC-LR) in the aquatic environment may disturb thyroid hormone (TH) homeostasis. It is not clear how MC-LR affects downstream biological processes after TH disturbance. After exposure to 50, 100, 200 and 400 μg/L MC-LR for 24, 48, 72, or 96 h, alterations of the TH metabolism of adult zebrafish at thyroxine (T4), triiodothyronine (T3) levels, and iodothyronine deiodinase (Dio) activity, were observed. After exposure to MC-LR at 400 μg/L, T3 and T4 levels decreased significantly in females (p 0.05) and returned to normal levels at 96 h. In males, T4 levels were not significantly different between groups. The expression of corticotropin releasing hormone, thyroid-stimulating hormone beta subunit, transthyretin, sodium/iodide cotransporter, thrombopoietin, thyroid hormone receptor alpha and beta changed, but not in a dose-dependent manner. Acute MC-LR exposure induced a negative feedback regulation of the hypothalamic-pituitary-thyroid axis in adult zebrafish, and females were more sensitive than males. In conclusion, acute MC-LR exposure disrupted the TH metabolism by altering Dio activity and gene expression of the HPT axis; these changes may affect the complement system through regulation of c9 mRNA synthesis.

Polybrominated diphenyl ethers (PBDEs) have the potential to disturb the thyroid endocrine system in vertebrates, but little is known about the disruptive effects of PBDEs on marine bivalves. In this study, we first examined the effects of BDE-47 exposure on growth of juvenile manila clams Ruditapes philippinarum. The result showed that 1.0 and 10 μg L(-1) BDE-47 had adverse effects on 14-d shell-length growth of juvenile clams. Then, one-year-old adult clams were exposed to 0, 0.1 and 1 μg L(-1) BDE-47 for 15 d. BDE-47 (1 μg L(-1)) exposure caused significant decreases of total T4 (thyroxine) by 40% and T3 (3,5,3'-triiodothyronine) by 75% concentrations in haemolymph of the clams. Transcription of genes involved in thyroid hormone synthesis and metabolism were also studied by quantitative RT-PCR. Gene expression levels of sodium iodide symporter (rp-NIS), iodothyronine deiodinase (rp-Deio) and thyroid peroxidase (rp-TPO) were increased in a dose-dependent manner at day 5 and day 10, while monocarboxylate transporter 8 (rp-Mct8) was downregulated at day 5, day 10 and day 15. The effect and preliminary mechanism observed in the present study were consistent with the results from previous studies on rodent and fish, implying that exposure to BDE-47 may pose threat to thyroid hormone homeostasis in bivalves through thyroid synthesis and metabolism pathways. This study may provide a first step towards understanding of the thyroid function disruptive effects of PBDEs on marine bivalves and the underlying mechanism across taxonomic groups and phyla.

This study investigated the effects of microcystin (MC) on the regulation of thyroid hormone (TH) metabolism in juvenile zebrafish exposed to MC-LR. The results showed that acute MC-LR exposure at concentrations ranging from 50 μg/L to 400 μg/L led to significant reductions in thyroxine (T4) and triiodothyronine (T3) levels in juvenile zebrafish. The transcription levels of genes involved in TH synthesis, such as corticotropin-releasing hormone (crh), thyroid-stimulating hormone (tsh), thyroid peroxidase (tpo) and transthyretin (ttr), were significantly decreased followed by an increase after MC-LR exposure. Transcription of the TH nuclear receptors (tr-α and tr-β) was significantly reduced during the exposure period. Moreover, the activities of iodothyronine deiodinase type Ⅰ (ID1) and iodothyronine deiodinase type Ⅱ (ID2) showed initially decreased and then increased trend, while the activity of iodothyronine deiodinase type Ⅲ (ID3) significantly decreased during MC-LR exposure. In addition, the effect of MC-LR on deiodinase activities and T4 contents were important causes of the decreased T3 at the early exposure stage. These results indicated that acute MC-LR exposure significantly interfered with the transcription of genes related to TH synthesis, transport and metabolism, and affected normal function of the thyroid which leads to decrease of T4 and T3 in juvenile zebrafish. Therefore, the thyroid function is susceptible to interference by MC-LR, and it may cause adverse effects on the growth and development of juvenile zebrafish.

Chinese toad (Bufo gargarizans) tadpoles were exposed to nitrate (10, 50 and 100 mg/L NO3–N) from the beginning of the larval period through metamorphic climax. We examined the effects of chronic nitrate exposure on metamorphosis, mortality, body size and thyroid gland. In addition, thyroid hormone (TH) levels, type II iodothyronine deiodinase (Dio2) and type III iodothyronine deiodinase (Dio3) mRNA levels were also measured to assess disruption of TH synthesis. Results showed that significant metamorphic delay and mortality increased were caused in larvae exposed to 100 mg/L NO3–N. The larvae exposed to 100 mg/L NO3–N clearly exhibited a greater reduction in thyroxine (T4) and 3,5,3′-triiodothyronine (T3) levels. Moreover, treatment with NO3–N induced down-regulation of Dio2 mRNA levels and up-regulation of Dio3 mRNA levels, reflecting the disruption of thyroid endocrine. It seems that increased mass and body size may be correlated with prolonged metamorphosis. Interestingly, we observed an exception that exposure to 100 mg/L NO3–N did not exhibit remarkable alterations of thyroid gland size. Compared with control groups, 100 mg/L NO3–N caused partial colloid depletion in the thyroid gland follicles. These results suggest that nitrate can act as a chemical stressor inducing retardation in development and metamorphosis. Therefore, we concluded that the presence of high concentrations nitrate can influence the growth, decline the survival, impair TH synthesis and induce metamorphosis retardation of B. gargarizans larvae.

Nitrite has the potential to disturb thyroid hormone homeostasis, but little is known about the underlying mechanisms. In the present study, juvenile grass carp ( Ctenopharyngodon idellus ) were exposed to various concentrations of nitrite (0, 0.5, 1, 4, and 16 mg/L, respectively). Serum concentrations of triiodothyronine (T 3 ), thyroxine (T 4 ), free triiodothyronine (FT 3 ), free thyroxine (FT 4 ), 3,3,5ʹ-triiodothyronine (rT 3 ), thyroid-stimulating hormone (TSH), and the activity of iodothyronine deiodinases were assayed at 0, 12, 24, 48, and 96 h after exposure. It was found that acute nitrite exposure significantly altered the TH levels and iodothyronine deiodinase activities. The rT 3 levels were significantly increased in the treatment groups, whereas the concentrations of T 3 , FT 3 , FT 4 , and TSH decreased significantly. The concentration of T 4 was elevated in the lower-dose exposure group, but was reduced in the higher-dose exposure group. Increases in type I iodothyronine deiodinase (ID1) and type III iodothyronine deiodinase (ID3) activities were observed in the exposure groups. The activity of type II iodothyronine deiodinase (ID2) decreased at 12 and 24 h after exposure. A decrease of colloid in the thyroid follicles was observed in the exposure group. The results indicate that acute nitrite exposure has the potential to disturb the homeostasis of thyroid hormone metabolism, leading to a hypothyroidism state in the juvenile grass carp.