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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]

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]

The perfluorooctane sulfonate alternative, F–53B, induces multiple physiological defects but whether it can disrupt eye development is unknown. We exposed zebrafish to F–53B at four different concentrations (0, 0.15, 1.5, and 15 μg/L) for 120 h post-fertilization (hpf). Locomotor behavior, neurotransmitters content, histopathological alterations, morphological changes, cell apoptosis, and retinoic acid signaling were studied. Histology and morphological analyses showed that F–53B induced pathological changes in lens and retina of larvae and eye size were significantly reduced as compared to control. Acridine orange (AO) staining revealed a dose-dependent increase in early apoptosis, accompanied by upregulation of p53 , casp-9 and casp-3 genes. Genes related to retinoic acid signaling (aldh1a2), lens developmental (cryaa , crybb , crygn , and mipa) and retinal development (pax6 , rx1 , gant1 , rho , opn1sw and opn1lw) were significantly downregulated. In addition, behavioral responses (swimming speed) were significantly increased, while no significant changes in the neurotransmitters (dopamine and acetylcholine) level were observed. Therefore, in this study we observed that exposure to F–53B inflicted histological and morphological changes in zebrafish larvae eye, induced visual motor dysfunctions, perturbed retinoid signaling and retinal development and ultimately triggering apoptosis. [Display omitted] • F–53B induce small eye and histopathological abnormalities in larvae eye. • F–53B induce dose-dependent manner apoptosis in larvae eye. • mRNA levels involved in eye developmental were significantly changed. • F–53B induces locomotor behavior perturbed eye development disorders. [ABSTRACT FROM AUTHOR]

It has been reported that exposure to perfluorooctane sulfonates (PFOS) causes behavioral abnormalities in zebrafish larvae, but the possible mechanisms underlying these changes remain unexplored. In this study, zebrafish embryos (2 h postfertilization, 2-hpf) were exposed to PFOS at different concentrations (0, 0.032, 0.32 and 3.2 mg/L) for 120 h. Developmental endpoints and the locomotion behavior of larvae were evaluated. Reactive oxygen species (ROS) levels, dopamine contents, several genes and proteins related to neurodevelopment and dopamine signaling were examined. Our results indicate that increased ROS levels in the zebrafish larvae heads may be causally associated with neurodevelopment damage. Meanwhile, brain-derived neurotrophic factor (BDNF) and alpha1-Tubulin (α1-Tubulin) protein contents were significantly increased, which may be a compensatory mechanism for the impaired central nervous system. PFOS-induced locomotor hyperactivity was observed in the first light phase and dark phase at the 0.32 and 3.2 mg/L of PFOS. Upregulation of dopamine-related genes tyrosine hydroxylase (th) and dopamine transporter (dat) associated with increased dopamine contents in the 3.2 mg/L of PFOS. In addition, protein expression of TH and DAT were noted at the 0.32 and 3.2 mg/L of PFOS concentrations. Our results suggested that PFOS induces neurobehavioral changes in zebrafish larvae, possibly by perturbing a dopamine signaling pathway. In addition, PFOS induced development damage, such as increased malformation rate and shorter body length. [Display omitted] • PFOS induced ROS generation in larvae head. • PFOS induced neurobehavioral in larvae. • mRNA and protein levels involved in dopamine pathway were significantly changed. • PFOS induced neurobehavioral in larvae, which might be to a dopamine pathway. [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]

• 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]

The adverse effects of triphenyltin (TPT) on aquatic systems have attracted much attention because TPT is widely used and prevalent in aquatic environments. Here, zebrafish embryos/larvae were exposed to TPT (0, 0.039, 0.39, and 3.9 nM; 0, 15, 150 and 1500 ng/L) for 7 or 14 days to determine its toxic effects on the hypothalamic–pituitary–thyroid (HPT) axis. The results showed that whole-body total T4 and T3 levels were significantly decreased, which was accompanied by the significant upregulation of the expression of the dio1 , dio2 and ugt1ab genes after exposure to TPT for 7 and 14 days. Genes related to thyroid hormone synthesis (crh , tshβ , nis, tpo and tg) were upregulated at both 7 and 14 days after TPT exposure. This might have been due to the positive feedback regulation of the HPT axis, which is caused by a decrease in thyroid hormone in the whole body in zebrafish. In addition, the survival rates and body lengths were reduced after treatment with TPT for 7 and 14 days. This indicated that TPT caused adverse effect on the development of zebrafish embryos/larvae. In summary, the results suggested that TPT caused thyroid disruption and developmental toxicity in zebrafish larvae. Unlabelled Image • TPT exposure caused developmental toxicity in zebrafish larvae. • The gene expression patterns of the HPT axis were changed after TPT exposure. • TPT significantly decreased whole-body thyroid hormone levels. • TPT at environmental dose caused thyroid disruption in zebrafish larvae. [ABSTRACT FROM AUTHOR]