Sex-specific thyroid disruption caused by phenanthrene in adult zebrafish (Danio rerio).

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.

Copper and Zinc Treatments Alter the Thyroid Endocrine System in Zebrafish Embryos/Larvae.

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.

Variations of trophic structure and niche space in fish community along a highly regulated subtropical large river.

The trophic interactions between consumers and resources play a vital role in the stability of communities. In river systems, fragmentation of natural habitats and environmental changes alters the energy basis and community composition, consequently leading to variations in the community's trophic structure and niche space. However, our understanding of how the trophic structure responds to environmental changes is still very limited. Here, based on stable isotope data, we explored and compared trophic positions (TPs), community-wide trophic metrics, and isotope niche space of fish communities in three reaches with different hydrogeomorphic conditions along a highly regulated subtropical river over three seasons. The community trophic structure and niche space showed notable spatiotemporal variations. Overall, the downstream reach had lower TPs, trophic diversity but higher trophic redundancy. The middle reach occupied a wider isotope niche space than other reaches, with the largest niche size during autumn. Furthermore, the niche overlap was relatively high in winter between reaches and in the downstream between seasons. The results implied a homogenization of feeding functional groups and energy flow pathways of species in the downstream community associated with the change of energy source and stability of hydrological conditions. The relationship between trophic structure and environmental factors suggested that the dam-induced alteration in hydrological-related aspects may drive the changes in the functional group composition, together with changes in energy basis, resulting in differences in the trophic structure of the community. The results of the present study deepen our understanding of how ecosystem functions respond to disturbance, thus contributing to improved ability to conserve river ecosystems.

Thyroid disruption and growth inhibition of zebrafish embryos/larvae by phenanthrene treatment at environmentally relevant concentrations.

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.

Sex-specific effects of triphenyltin chloride (TPT) on thyroid disruption and metabolizing enzymes in adult zebrafish (Danio rerio).

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 17ß-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.

Thyroid disruption and developmental toxicity caused by Cd2+ in Schizopygopsis younghusbandi larvae.

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 tshß) 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.

Thyroid disruption and developmental toxicity caused by triphenyltin (TPT) in zebrafish embryos/larvae.

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, tshß, 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.

Comparative thyroid disruption by o,p'-DDT and p,p'-DDE in zebrafish embryos/larvae.

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, tshß, 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.

Parental exposure to 2,2',4,4'5 - pentain polybrominated diphenyl ethers (BDE-99) causes thyroid disruption and developmental toxicity in zebrafish.

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.

Mitochondrial DNA sequence of ruffe (Gymnocephalus cernua).

The complete mitochondrial genome (mitogenome) of the Gymnocephalus cernua has been studied. The genome sequence was 16,614 bp in length, including the typical structure of 22 transfer RNA genes, 13 protein-coding genes, two ribosomal RNA genes, and the non-coding control region. The overall base composition of G. cernua mitogenome is 27.84% A, 27.60% T, 16.61% G, and 27.94% C, with a high A + T content of 55.45%. The complete mitochondrial genome of G. cernua provides basic genome data for relative studies on Perciformes.