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Cadmium (Cd2+) and mercury (Hg2+) are two kinds of non-essential heavy metals. Cd2+ and Hg2+ can cause thyroid disruption, but very few researchers have investigated the thyroid-disrupting effects of these metals on fish, specifically during their early developmental transition stage from embryos to larvae. In this study, wild-type zebrafish embryos were exposed to varying concentrations (contents) of Cd2+ (0, 10, 100, and 1000 μg/L) and Hg2+ (0, 0.1, 1, and 10 μg/L) for 120 h. Thereafter, the thyroid hormone contents and transcriptional changes in the genes, including thyroid stimulating hormone-β (tshβ), thyroglobulin (tg), sodium-iodide symporter (nis), thyroid peroxidase (tpo), transthyretin (ttr), thyroid hormone receptor-α and -β (thrα, thrβ), types I and II iodothyronine deiodinase (dio1, dio2), and uridine diphosphate glucuronosyltransferase 1 family a, b (ugt1ab) associated with the hypothalamic-pituitary-thyroid (HPT) axis were measured. Results showed that zebrafish embryos/larvae malformation rates were significantly higher in the Cd2+ and Hg2+ groups. A significant increase in the thyroxine (T4) concentration and a decrease in the triiodothyronine (T3) concentration were observed in the Cd2+-exposed zebrafish embryos/larvae. On the other hand, the T4 and T3 concentrations were observed to be significantly increased after Hg2+ exposure. Additionally, changes were noted in the expression patterns of the HPT axis-linked genes after Cd2+ and Hg2+ exposure. Based on the results of the principal component analysis (PCA), it was concluded that Cd2+ exposure significantly affected the thyroid endocrine system at a concentration of 100 μg/L, whereas Hg2+ exposure led to a thyroid disruption at a low concentration of 0.1 μg/L. Thus, this study demonstrated that exposure to Cd2+ and Hg2+ metal ions induced developmental toxicity and led to thyroid disruption in zebrafish embryos/larvae. [ABSTRACT FROM AUTHOR]

Copper (Cu2+) and zinc (Zn2+) are two kinds of heavy metals essential to living organisms. Cu2+ and Zn2+ at excessive concentrations can cause adverse effects on animals, but little is known about the thyroid-disrupting effects of these metals in fish, especially in the early developmental transition stage from embryos to larvae. Wild-type zebrafish embryos were used to expose to Cu2+ (0, 1.5, 15, and 150 μg/L) and Zn2+ (0, 20, 200, and 2000 μg/L) for 120 h. Thyroid hormone contents and transcriptional changes of the genes connected with the hypothalamic-pituitary-thyroid (HPT) axis were measured. Results showed that zebrafish embryos/larvae malformation rates were significantly increased in the Cu2+ and Zn2+ groups. Remarkably elevated thyroxine (T4) concentrations and reduced triiodothyronine (T3) concentrations were observed in Cu2+ and Zn2+ exposure fish. And the expression patterns of genes connected with the HPT axis were changed after Cu2+ and Zn2+ treatment. Based on principal component analysis (PCA) results, Zn2+ caused significant effects on the thyroid endocrine system at 200 μg/L, while Cu2+ resulted in thyroid disruption as low as 1.5 μg/L. In short, our study demonstrated that exposure to Cu2+ and Zn2+ induced developmental toxicity and thyroid disruption to zebrafish embryos/larvae. [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbons (PAHs) are well-known contaminants with widespread distribution in environment and food. Phenanthrene is one of the most abundant PAHs in food and aquatic environment and generates reproductive and developmental toxicity in zebrafish. Nonetheless, whether phenanthrene caused sex-specific thyroid disruption in adult zebrafish is unclear. To determine this, adult zebrafish (male and female) were treated with phenanthrene (0, 0.85, 8.5, and 85 μg/L) for 60 days. After the treatment period, we assessed the concentrations of thyroid hormones (THs) and expression levels of genes in the hypothalamic-pituitary-thyroid (HPT) axis. The results showed that phenanthrene exposure can lead to thyroid disruption in both male and female zebrafish. Exposure to phenanthrene dramatically reduced the levels of L-thyroxine (T4) and L-triiodothyronine (T3) in both male and female zebrafish, with a similar trend in both. However, the genes expression profiles of hypothalamic-pituitary-thyroid (HPT) axis were sex-specific. In all, the present study demonstrated that phenanthrene exposure could result in sex-specific thyroid disruption in adult zebrafish. [Display omitted] • Phenanthrene exposure caused thyroid disruption in both male and female zebrafish. • Phenanthrene exposure deduced thyroid hormones regardless of gender. • The genes expression profiles of HPT axis were sex-specific after phenanthrene exposure. [ABSTRACT FROM AUTHOR]

N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine (6PPD) is used as a ubiquitous rubber antioxidant worldwide and has been shown to be potentially toxic to aquatic organisms. In this study, zebrafish embryos were exposed to 6PPD for five days starting at two hours post-fertilization at concentrations of 0, 0.0022, 0.022, and 0.22 mg/L to investigate its effects on embryonic development, the growth hormone/insulin-like growth factor (GH/IGF) axis, and the hypothalamic-pituitary-thyroid (HPT) axis. The results showed that the 96 h LC50 of 6PPD was 2.2 mg/L. 6PPD exposure decreased hatchability, lowered autonomous movement, reduced body length in zebrafish embryos and caused deformities. The hormones levels and the expression of genes related to GH/IGF and HPT axis were altered after exposure to 6PPD in zebrafish larvae. These results indicated that the GH/IGF and HPT axis was disturbed. Moreover, treatment of 6PPD produced oxidative stress in zebrafish embryos. Overall, the present study thus demonstrated that exposure to 0.22 mg/L 6PPD caused developmental toxicity and disrupted the GH/IGF and HPT axis of zebrafish, which could be responsible for developmental impairment and growth inhibition. [Display omitted] • The 96 h LC50 of 6PPD was 2.2 mg/L. • 6PPD exposure cause developmental toxicity in zebrafish embryos/larvae. • The developmental toxicity induced by 6PPD is the result of GH/IGF endocrine and thyroid system disruption. • 6PPD exposure affected the oxidative stress state of zebrafish embryos/larvae. [ABSTRACT FROM AUTHOR]

• Phenanthrene accumulated rapidly and then quickly decreased in zebrafish embryos/larvae. • Phenanthrene caused thyroid disruption via the HPT axis. • Phenanthrene caused growth inhibition via the GH/IGF-1 axis. Phenanthrene induces reproductive and developmental toxicity in fish, but whether it can disrupt the thyroid hormone balance and inhibit growth had not been determined to date. In this study, zebrafish embryos were exposed to phenanthrene (0, 0.1, 1, 10 and 100 μg/L) for 7 days. The results of this experiment demonstrated that phenanthrene induced thyroid disruption and growth inhibition in zebrafish larvae. Phenanthrene significantly decreased the concentration of l -thyroxine (T4) but increased that of 3,5,3′- l -triiodothyronine (T3). The expression of genes related to the hypothalamic-pituitary-thyroid (HPT) axis was altered in zebrafish larvae exposed to phenanthrene. Moreover, phenanthrene exposure significantly increased the malformation rate and significantly reduced the survival rate and the body length of zebrafish larvae. Furthermore, phenanthrene significantly decreased the concentrations of growth hormone (GH) and insulin-like growth factor-1 (IGF-1). Changes observed in gene expression patterns further support the hypothesis that these effects may be related to alterations along the GH/IGF-1 axis. In conclusion, our study indicated that exposure to phenanthrene at concentrations as low as 0.1 μg/L resulted in thyroid disruption and growth inhibition in zebrafish larvae. Therefore, the estimation of phenanthrene levels in the aquatic environment needs to be revisited. [ABSTRACT FROM AUTHOR]

Triphenyltin (TPT) is widely used and commonly found in a water environment, so its effects on aquatic systems are of great concern. This study aimed to reveal the effects of chronic parental exposure of TPT on thyroid disruption and growth inhibition in zebrafish. Adult zebrafish (F0 generation) were exposed to environmentally relevant concentrations (1, 10, and 100 ng/L) of TPT for 60 days, and the larvae (F1 generation) were tested without TPT treatment. Results demonstrated that parental exposure to TPT disrupts thyroid function in zebrafish offspring: serum thyroxine (T4) significantly decreased, while serum 3,5,3′-triiodothyronine (T3) increased, and several genes involved in the hypothalamic–pituitary–thyroid (HPT) axis were down-regulated. In addition, we observed developmental abnormalities in the larvae, demonstrated by a significantly altered hatching rate, malformation rate, body length, heart rate, and survival rate, as well as down-regulation of genes involved in the growth hormone/insulin-like growth factor (GH/IGF) axis. Therefore, parental exposure to TPT induces toxicity in fish offspring through perturbation of the HPT and GH/IGF axes. • Parental exposure to TPT to a zebrafish model was conducted. • Embryonic developmental inhibition was observed in offspring larvae. • GH/IGF axis was disordered by exposure of TPT. [ABSTRACT FROM AUTHOR]

• TPT exposure caused thyroid disruption in zebrafish. • TPT exposure changed the liver metabolizing enzymes in zebrafish. • Thyroid disruption and detoxifying enzyme capacities changed were sex-specific in zebrafish. Although organotin compounds are known to disturb thyroid signaling and antioxidant defense system, the sex-differences underlying these effects of triphenyltin chloride (TPT) in fish remain unclear. To understand these differences, adult zebrafish (Danio rerio) were exposed to different concentrations of TPT (0, 10, 100, or 1000 ng/L) for 28 days. Female zebrafish exposed to TPT showed significantly increased thyroxine (T4) content and decrease triiodothyronine (T3) content, possibly due to downregulation of deiodinase (dio2) and uridine diphosphate glucuronosyl transferase (ugt1ab). However, decreased T4 and T3 contents in male zebrafish accompanied with upregulation of dio1 , dio2 and ugt1ab. TPT exposure can lead to sex-specific thyroid disruption in adult zebrafish via alterations the Hypothalamus-pituitary-thyroid-liver axis. In addition, the gene expression levels of metabolizing enzymes, such as cyp1b , cyp1c , gpx1a , or sult1st1 were also to vary in a sex-dependent manner in adult zebrafish liver. Downregulation of cyp19a and cyp19b and decreased 17β -estradiol (E2) contents were detected in both female and male zebrafish. Therefore, a sex-specific of thyroid disruption response after TPT exposure was observed in adult zebrafish, possibly due to inherent in female or males detoxifying enzyme capacities. [ABSTRACT FROM AUTHOR]

Although polybrominated diphenyl ethers (PBDEs) are known to disturb thyroid hormone signaling, the mechanisms underlying the effects of 2,2′,4,4′5 - pentain polybrominated diphenyl ethers (BDE-99) in fish remain unclear. In order to reveal these mechanisms, adult zebrafish (Danio rerio) were exposed to different concentrations of BDE-99 (0, 0.5, 5, or 50 μg/L) for 28 days and spawned by mating naturally in clean water (without BDE-99). Females exposed to BDE-99 showed significantly lowered thyroxine (T4) levels. Expression of transthyretin (ttr) and uridine diphosphate glucuronosyl transferase (ugt1ab) were down-regulated and up-regulated, respectively. Triiodothyronine (T3) levels in the 0.5 μg/L BDE-99 exposure group was significantly increased. Males showed significantly increased T3 levels, and lowered T4 levels, which were associated with up-regulated and down-regulated expression of deiodinase 2 (deio2) and ugt1ab , respectively. Exposure of adult zebrafish to BDE-99 lead to significantly increased T4 in the 0.5 μg/L BDE-99 exposure group, but in the 50 μg/L BDE-99 exposure group there was significantly reduced T4 in F1 larvae and altered mRNA transcription in the hypothalamic-pituitary-thyroid-liver (HPTL) axis. The offspring also showed reduced survival rates, and body length and elevated malformation rates. This study is the first in zebrafish to show that parental zebrafish exposure to BDE-99 can lead to developmental toxicity and thyroid disruption in the offspring. • Chronic exposure to BDE-99 in a zebrafish model was tested. • BDE-99 exposure causes thyroid endocrine disruption in the adult zebrafish. • BDE-99 exposure causes thyroid endocrine disruption and developmental toxicity in offspring larvae. [ABSTRACT FROM AUTHOR]

• o,p' -DDT and p,p′- DDE cause developmental toxicity in zebrafish larvae. • o,p' -DDT exposure significantly increased whole-body thyroid hormone levels. • p,p′- DDE exposure significantly decreased whole-body thyroid hormone levels. • The gene expression patterns of HPT axis were changed after exposure to either o,p' -DDT or p,p′ -DDE. 1,1-Trichloro-2-(p-chlorophenyl)-2-(o-chlorophenyl) ethane (o,p' -DDT) and 1,1-dichloro-2,2-bis (p-chlorophenyl)-ethylene (p,p′- DDE) cause thyroid disruption, but the underlying mechanisms of these disturbances in fish remain unclear. To explore the potential mechanisms of thyroid dysfunction caused by o,p' -DDT and p,p′- DDE, thyroid hormone and gene expression levels in the hypothalamic-pituitary-thyroid (HPT) axis were measured, and the developmental toxicity were recorded in zebrafish larvae. Zebrafish embryos/larvae were exposed to o,p' -DDT (0, 0.28, 2.8, and 28 nM; or 0, 0.1, 1, and 10 μg/L) and p,p′- DDE (0, 1.57, 15.7, and 157 nM; or 0, 0.5, 5, and 50 μg/L) for 7 days. The genes related to thyroid hormone synthesis (crh , tshβ , tg , nis and tpo) and thyroid development (nkx2.1 and pax8) were up-regulated in both the o,p' -DDT and p,p′- DDE exposure groups. Zebrafish embryos/larvae exposed to o,p' -DDT showed significantly increased total whole-body T4 and T3 levels, with the expression of ugt1ab and dio3 being significantly down-regulated. However, the p,p′- DDE exposure groups showed significantly lowered whole-body total T4 and T3 levels, which were associated with up-regulation and down-regulation expression of the expression of dio2 and ugt1ab , respectively. Interestingly, the ratio of T3 to T4 was significantly decreased in the o,p' -DDT (28 nM) and p,p′- DDE (157 nM) exposure groups, suggesting an impairment of thyroid function. In addition, reduced survival rates and body lengths and increased malformation rates were recorded after treatment with either o,p' -DDT or p,p′- DDE. In summary, our study indicates that the disruption of thyroid states was different in response to o,p' -DDT and p,p′ -DDE exposure in zebrafish larvae. [ABSTRACT FROM AUTHOR]