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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]

Vigilin, a highly conserved protein from yeast to mammals, is a multifunctional protein in eukaryotic organisms. One biological function of vigilin is to stabilize the expression level of vitellogenin (VTG). This study aimed to develop vigilin as a new estrogen-inducible biomarker that correlates with the widely applied estrogen-inducible biomarker VTG and expand the ability to detect it in various species. Here, a recombinant monoclonal antibody with high specificity against the conserved C-terminal region of vigilin from zebrafish ( Danio rerio ) was successfully isolated from a phage display antibody library and found to recognize vigilin proteins from multiple vertebrate species. The effect of 17α-ethinylestradiol (EE2) on vigilin expression in the liver of zebrafish and juvenile crucian carp ( Carassius auratus ) was investigated. Although vigilin mRNA was expressed in all tissues analyzed from male zebrafish, vigilin protein was detected exclusively in the testis of male zebrafish, as well as the liver of female zebrafish and juvenile crucian carp at a lower level without exposure to EE2. Significant induction of vigilin mRNA by exposure to EE2 was observed in the liver and testis of male zebrafish, even at a low dose of 6.25 ng/L (21.09 pmol/L). In Hela cells, the expression of vigilin coincided with high protein synthesis activity but not dose-dependently by EE2 exposure. Therefore, the recombinant antibody may be used as a detection tool to screen for mammalian cell lines or organs with estrogen-inducible expression of vigilin. [ABSTRACT FROM AUTHOR]

Highlights: [•] Vitellogenin was present in the liver as well as in various extrahepatic tissues. [•] The induction of vitellogenin by EE2 in skin and eye was in a dose-dependent manner. [•] The induction of vitellogenin by EE2 in skin and eye was in a time-dependent manner. [•] Skin and eye are alternative tissues for vitellogenin analysis as biomarker. [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]

The adverse influences of triphenyltin (TPT) on aquatic system have been of great concern due to their widespread use and ubiquity in water environment. Here, zebrafish larvae (7 days after hatching) were exposed to TPT for 14 days to study its toxicity on the antioxidant system, energy metabolism and the expression of genes related to physiological stress. Results shows that the oxidative stress was generated in fish larvae exposed to TPT with higher concentrations (10 and/or 100 ng/l), and the energy metabolic parameters (RNA/DNA ratio, Na + -K + -ATPase) were significantly inhibited in fish exposed to 100 ng/l TPT. Additional, the expression levels of genes related to physiological stress were up-regulated in a dose-dependent manner, including heat shock protein70 (hsp70) and metallothionein (mt). Moreover, the PERK–eIF2α pathway was found as the main branch activated by TPT exposure in fish larvae. Thus, TPT-induced antioxidant responses, energy metabolism disorder and physiological stress in fish larvae were reflected by the parameters measured, which could provide some useful information for full understanding the exact mechanisms of TPT toxicity. Individual variations of biochemical and molecular parameters in zebrafish larvae exposed to TPT by using PCA. Unlabelled Image • Exposure of TPT caused oxidative stress in fish larvae. • Energy metabolism was modulated in fish larvae under TPT stress. • Environmental level of TPT could result in the physiological stress in fish larvae. [ABSTRACT FROM AUTHOR]

In recent years, the adverse effects of cadmium (Cd2+) on aquatic systems have attracted much attention because Cd2+ can induce endocrine disorders and toxicity in aquatic organisms at low levels. However, its effects on the thyroid system in native fish in Lhasa are still unclear. In the present study, Schizopygopsis younghusbandi larvae were exposed to Cd2+ (0.25, 2.5, 25 or 250 μg/L) for 7 or 14 days to determine its toxic effects on thyroid function. 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 and dio2 genes after exposure to Cd2+ for 7 or 14 days. Genes related to thyroid hormone synthesis (crh and tshβ) were upregulated after both 7 and 14 days of Cd2+ exposure, possibly due to the negative feedback regulation of the hypothalamic-pituitary-thyroid (HPT) axis caused by a decrease in thyroid hormone. In addition, survival rates and body lengths were reduced after treatment with Cd2+. This suggests that Cd2+ caused developmental toxicity in Schizopygopsis younghusbandi larvae. An integrated assessment of biomarker response (IBR) showed that there were dose-dependent and time-dependent effects of Cd2+ exposure on Schizopygopsis younghusbandi larvae. Schizopygopsis younghusbandi larvae were sensitive to Cd2+, which caused adverse effects at a concentration as low as 2.5 μg/L. In summary, the results indicated that Cd2+ causes thyroid disruption and developmental toxicity in Schizopygopsis younghusbandi larvae and that wild Schizopygopsis younghusbandi larvae living in the Lhasa River are at potential ecological risk. Unlabelled Image • Cd2+ exposure causes developmental toxicity in Schizopygopsis younghusbandi larvae. • Cd2+ exposure causes thyroid disruption in Schizopygopsis younghusbandi larvae. • Schizopygopsis younghusbandi larvae face ecological risks in the Lhasa River. [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]