Morphological variation in Schizothorax oconnori, Schizothorax waltoni (Teleostei: Cyprinidae: Schizothoracinae), and their natural hybrids from the middle Yarlung Zangbo River, Tibet.

The morphological variation in Schizothorax oconnori, Schizothorax waltoni, and their natural hybrids was examined using conventional and image-based analysis approaches. In total, 38 specimens of S. oconnori, 35 of S. waltoni, and 37 natural hybrids were collected from the Shigatse to the Lhasa section of the Yarlung Zangbo River during June and July 2021. A total of 21 morphometric, 4 meristic, and 27 truss variables were employed for the classification of S. oconnori, S. waltoni, and natural hybrids. Principal component analysis (PCA) and factor analysis (FA), as well as discriminant function analysis (DFA) and cluster analysis (CA), were conducted to identify differences based on traditional and truss measurements. Four principal components explained 75.92% of the variation among the morphometric characters, while five principal components accounted for 79.69% of the variation among the truss distances. FA results showed that factor 1 was associated with head shape, and factor 2 was associated with fins based on morphometric characters. Among the truss characters, factor 1 was related to head shape, and factor 2 was related to chest shape. In DFA, morphometric measurements achieved higher accuracy (100%) compared to truss distances (94.55%). The head morphology of hybrids exhibited intermediate traits between S. oconnori and S. waltoni. Both morphometry-based and truss-based clustering indicated that the morphology of natural hybrids leaned toward S. oconnori. In conclusion, the combination of morphometric and truss analysis is beneficial for classifying S. oconnori, S. waltoni, and their natural hybrids. The presence of natural hybrids could be considered an evolutionary response to the differentiation of nutritional and spatial niches in the middle Yarlung Zangbo River.

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.

Environmentally relevant concentrations of tris (1,3-dichloro-2-propyl) phosphate induce growth inhibition and oxidative stress in silver carp (Hypophthalmichthys molitrix) larvae.

Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP), widely applied as flame retardant into a variety of products, can be physically leached out to the aquatic environment. Measurable values of TDCIPP have been found in the environment and within biota. Many toxicological assessments have shown that TDCIPP could cause developmental toxicity and oxidative stress in fish. In this study, we focused on the effects of TDCIPP on the growth and oxidative stress of an important commercial fish species in China, silver carp (Hypophthalmichthys molitrix). Fish larvae was exposed to environmentally relevant concentrations (0.05, 0.5, 5 and 50 µg/L) of TDCIPP for 7, 14 and 28 days. Simultaneously, the transcription levels of genes associated with the growth hormone/insulin-like growth factor (GH/IGF) axis and the antioxidative enzymes were examined. The body length and body mass of silver carp larvae decreased significantly only under exposure to 5 and 50 µg/L of TDCIPP at 14 days compared with the control group, while differences on those paraments were observed at 0.05, 0.5, 5 and 50 µg/L when larvae were exposed for 28 days. The observation evidenced the time- and dose- dependent growth inhibitions caused by TDCIPP on silver carp larvae. Exposure to TDCIPP also decreased the contents of GH and IGF1 in fish attended by significant down-regulation of gh and igf1. Moreover, TDCIPP up-regulated the expression of cat, sod1 and gstt followed by an increase of the activities of catalase (CAT) and superoxide dismutase (SOD) and the levels of malondialdehyde (MDA) and glutathione (GSH), but the activities of glutathione peroxidase (GPX) were decreased. These results suggested that growth inhibition and oxidative stress co-occurred in silver carp larvae after exposure to environmentally relevant concentrations of TDCIPP accompanied by the abnormal expression of genes which associated with the GH/IGF axis and antioxidative enzymes.

IPPD-induced growth inhibition and its mechanism in zebrafish.

N-isopropyl-N-phenyl-1,4-phenylenediamine (IPPD) is used as a ubiquitous antioxidant worldwide, it is an additive in tire rubber easily discharged into the surrounding environment. At present, there is no study concerning the subacute toxicity of IPPD on fish. We used zebrafish embryos (2 h post-fertilization) exposed to IPPD for 5 days at concentrations of 0, 0.0012, 0.0120 and 0.1200 mg/L to investigate its toxic effects of embryonic development, disruption of growth hormone/insulin-like growth factor (GH/IGF) and hypothalamic-pituitary-thyroid (HPT) axis. The results showed that IPPD exposure decreased hatchability, weakened movement ability, reduced body length, and caused multiple types of deformities in zebrafish embryos. The expression of genes involved to GH/IGF and HPT axis were altered after exposure to IPPD in zebrafish larvae. Meanwhile, exposure to IPPD significantly decreased thyroxine (T4) and 3,5,3'-triiodothyronine (T3) contents in larvae, which indicated that HPT axis was in a disturbed state. Moreover, treatment of IPPD decreased the enzymatic activities of superoxide dismutase (SOD) and catalase (CAT) as well as levels of glutathione (GSH). While the contents of malondialdehyde (MDA) were elevated after exposure to IPPD. The present study thus demonstrated that IPPD induced oxidative stress, caused developmental toxicity and disrupted the GH/IGF and HPT axis of zebrafish, which could be responsible for developmental impairment and growth inhibition.

Environmentally relevant concentrations of mercury inhibit the growth of juvenile silver carp (Hypophthalmichthys molitrix): Oxidative stress and GH/IGF axis.

Mercury (Hg) is a global environmental contaminant, and excessive mercury levels in water can adversely affect the growth of fish. Silver carp (Hypophthalmichthys molitrix) is one of the important freshwater aquaculture fish in China, and its natural resources have been critically declining. However, the effects of Hg2+ exposure on the growth hormone/insulin-like growth factor (GH/IGF) axis and its toxic mechanism are still unclear. In this study, we systematically evaluated the bioaccumulation, histomorphology, antioxidant status, hormone levels, and GH/IGF axis toxicity of juvenile silver carp after exposure to environmental-related concentrations of Hg2+ (0, 0.05, 0.5, 5, and 50 µg/L) for 28 days. Results showed that the Hg2+ bioaccumulation in the liver increased with a rise in Hg2+ concentration and time of exposure. The body length (BL), body weight (BW), weight growth rate (WGR) and specific growth rate (SGR) all decreased after Hg2+ exposure. The serum levels of growth hormones (GH and IGF) and thyroid hormones (T3 and T4) were significantly decreased, and the expressions of GH/IGF axis-related genes were significantly downregulated after 7, 14, and 28 days of Hg2+ exposure. Correlations between the growth parameters and growth hormones or expression of genes in GH/IGF axis further suggested that environmentally relevant concentrations of Hg2+ could have adverse effects on growth. In addition, with increasing Hg2+ exposure, superoxide activities of dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST)and levels of reduced glutathione (GSH) and malondialdehyde (MDA) were significantly increased, whereas the activity of glutathione peroxidase (GPx) significantly decreased and oxidative stress-related gene significantly changed. Liver lesions were mainly characterized by inflammatory cell infiltration, hepatocyte necrosis and fat vacuolation after exposure to Hg2+. Taken together, the results indicate that Hg2+ exposure leads to growth inhibition and oxidative stress in juvenile silver.

Exposure to N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD) affects the growth and development of zebrafish embryos/larvae.

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.

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.

Lead impaired immune function and tissue integrity in yellow catfish (Peltobargus fulvidraco) by mediating oxidative stress, inflammatory response and apoptosis.

Lead (Pb) widely exists in the water environment and has severe toxic effects on aquatic organisms. The yellow catfish (Pelteobagrus fulvidraco) is one of the most important commercial species in China, and moreover, its natural populations are declining with the degradation of environmental water quality. However, little is known about the toxic effects of Pb on its immune organs. This study was performed to determine waterborne Pb exposure on bioaccumulation, histomorphology, antioxidant status, apoptotic and immune response in the head kidney and spleen of yellow catfish. Experimental fish were randomly allocated into twelve tanks (3 tanks per group), and the Pb concentrations of the four groups were 0, 5, 50, and 500 µg/L, respectively. The results reflected that the Pb bioaccumulation of the head kidney and spleen increased with increasing Pb exposure dose and time. Severe histological alterations in the head kidney and spleen were observed at concentration 500 ug/L. With increasing Pb exposure concentrations, the plasma activity of superoxide dismutase (SOD) and catalase (CAT) significantly increased after exposure 7 days and 14 days, and the levels significantly decreased after exposure 28 days. The change trend of glutathione (GSH) levels was opposite to that of SOD and CAT at corresponding exposure time. The plasma malondialdehyde (MDA) levels together with the activities of plasma alkaline phosphatase (AKP) and acid phosphatase (ACP) increased significantly with the increasing Pb concentrations. In contrast, the levels of lysozyme (LYZ), complement 3 (C3) and immunoglobulin M (IgM) decreased significantly with increasing Pb concentrations. Moreover, Pb exposure induced transcriptional upregulation of heat shock protein 70 (hsp70), metallothionein (mt), sod, cat, interleukin-10 (il-10), transforming growth factor-ß (tgf-ß), and tumor necrosis factor-α (tnf-α), bcl-2-associated X protein (bax), and cysteinyl aspartate specific proteinase -9 (caspase-9), genes in the head kidney and spleen tissues, while downregulating the levels of the lyz, c3, igm and B-cell lymphoma-2 (bcl-2) genes. Our data provide evidence that Pb impaired immune function and tissue integrity in yellow catfish through oxidative stress, inflammatory and apoptosis, and the results can serve as reference data to better protect water environments from Pb eco-toxicants.

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.

Effects of 27 natural products on drug metabolism genes in channel catfish (Ictalurus punctatus) cell line.

Pregnane X receptor (PXR) as a ligand dependent transcription factor, is capable of regulating gene expression of cytochromes P450 and transporters involved in xenobiotic/drug metabolism and elimination. Due to the species differences in the regulatory specificity of PXR, gene regulation should not be extrapolated from mammal to fish without research data.The aim of present study was to investigate the effect of 27 natural products on PXR, CYP3A30 and MDR1 genes in channel catfish (Ietalurus punetaus) kidney cells (CC-K). The results showed that bisdemethoxycurcumin, glycyrrhetnic acid, rotenone, artemisinin, dihydroartemisinin, ligustilide and matrine strongly induced the mRNA levels of PXR. Additionally, the up-regulation of CYP3A30 gene ran parallel with PXR gene after the treatment of demethoxycurcumin, glycyrrhetnic acid, artemisinin, matrine, baicalein, schisantherin A, ligustilide, and dihydroartemisinin. Moreover, we found that natural products schisandrin A, schisandrin B, schisandrol A, and schisandrol B significantly up-regulated the mRNA level of MDR1 gene.Our work with a view to provide experimental data support for further research, which will make for the rational application of natural products in channel catfish, such as to avoid adverse herb-drug interactions or accelerating the residue elimination of chemical medicine.

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.

Parental exposure to triphenyltin inhibits growth and disrupts thyroid function in zebrafish larvae.

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.

Effects of low concentrations of triphenyltin on neurobehavior and the thyroid endocrine system in zebrafish.

In the present study, to evaluate neurobehavioral toxicity and the thyroid-disrupting effects of environmental levels of triphenyltin (TPT), the zebrafish larvae were exposed to 1, 10 and 100 ng/l TPT. In the neurobehavioral assay, increased levels of dopamine and serotonin, decreased content of nitric oxide, inhibited activities of acetylcholinesterase and monoamine oxidase were observed in the whole body of zebrafish larvae after TPT treatment, as well as the serious abnormal non-reproductive behavior. Moreover, the whole-body the T4 levels were markedly decreased significantly, whereas T3 levels were not significantly changed under TPT stress. In addition, TPT exposure significantly changed the expression levels of genes related to thyroid system, including corticotropin-releasing hormone gene crh, thyroid-stimulating hormone gene tshß, thyroglobulin gene tg, sodium/iodide symporter gene nis, thyroid hormone nuclear receptor trα, isoform trß, types I deiodinase gene dio1and types II deiodinase gene dio2. The regulated responsiveness of thyroid hormone and related genes expression levels suggested that TPT could induce the thyroid disrupting effects in zebrafish larvae. Therefore, our results provide new aspects of TPT as an endocrine disrupting chemical.

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.

Triphenyltin exposure alters the antioxidant system, energy metabolism and the expression of genes related to physiological stress in zebrafish (Danio rerio).

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.

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.

Effect of Tributyltin, Cadmium, and Their Combination on Physiological Responses in Juvenile Grass Carp.

Tributyltin (TBT) and cadmium (Cd) are two common pollutants in aquatic environments. This study was designed to examine the physiological responses of juvenile Grass Carp Ctenopharyngodon idella to TBT, Cd, and their combination. Fish were apportioned into a control group, a TBT group (7.5 µg/L), a Cd group (2.97 mg/L), and a TBT-Cd group (7.5 µg/L TBT, 2.97 mg/L Cd(2+)) for 7 d. The following activities were measured: Na(+),K(+)-ATPase in gill tissues; nitric oxide synthase (NOS), acetylcholinesterase (AChE), and monoamine oxidase (MAO) in brain tissues; and lipid peroxidation (LPO), malondialdehyde (MDA), total antioxidative capacity (T-AOC), and glutathione (GSH) in liver tissues. Cadmium-induced stress was suggested by alterations in antioxidant responses (MDA, LPO, and T-AOC) and neurological parameters (AChE, MAO, and NOS). Cadmium also induced Na(+),K(+)-ATPase and GSH activity. Compared with the responses among the Cd group, the combination of TBT and Cd not only decreased the level of GSH and Na(+),K(+)-ATPase but also increased the levels of MDA, LPO, AChE, MAO, and NOS. These results suggest that a combination of TBT and Cd could reduce the adverse effects of Cd on Grass Carp. However, the exact mechanisms for the combined effects TBT and Cd on these biomarkers require further investigation. Received September 28, 2015; accepted April 17, 2016.