Identification and functional characterization of a superoxide dismutase (CuZnSOD) from Pinctada fucata martensii.

Copper/zinc superoxide dismutase (Cu/Zn-SOD) can effectively eliminate reactive oxygen species (ROS)，avoid damage from O2 to the body, and maintain O2 balance. In this study, multi-step high-performance liquid chromatography (HPLC), combined with Mass Spectrometry (MS), was used to isolate and identify Cu/Zn-SOD from the serum of Pinctada fucata martensii (P. f. martensii) and was designated as PmECSOD. With a length of 1864 bp and an open reading frame (ORF) of 1422 bp, the cDNA encodes a 473 amino acid protein. The PmECSOD transcript was detected in multiple tissues by quantitative real-time PCR (qRT-PCR), with its highest expression level being in the gills. Additionally, the temporal expression of PmECSOD mRNA in the hemolymph was highest at 48 h after in vivo stimulation with Escherichia coli and Micrococcus luteus. The results from this study provide a valuable base for further exploration of molluscan innate immunity and immune response.

Gut pathobiome mediates behavioral and developmental disorders in biotoxin-exposed amphibians.

Emerging evidence suggests a link between alterations in the gut microbiome and adverse health outcomes in the hosts exposed to environmental pollutants. Yet, the causal relationships and underlying mechanisms remain largely undefined. Here we show that exposure to biotoxins can affect gut pathobiome assembly in amphibians, which in turn triggers the toxicity of exogenous pollutants. We used Xenopus laevis as a model in this study. Tadpoles exposed to tropolone demonstrated notable developmental impairments and increased locomotor activity, with a reduction in total length by 4.37%-22.48% and an increase in swimming speed by 49.96%-84.83%. Fusobacterium and Cetobacterium are predominant taxa in the gut pathobiome of tropolone-exposed tadpoles. The tropolone-induced developmental and behavioral disorders in the host were mediated by assembly of the gut pathobiome, leading to transcriptome reprogramming. This study not only advances our understanding of the intricate interactions between environmental pollutants, the gut pathobiome, and host health but also emphasizes the potential of the gut pathobiome in mediating the toxicological effects of environmental contaminants.

Differentiation and risk stratification of basal cell carcinoma with deep learning on histopathologic images and measuring nuclei and tumor microenvironment features.

BACKGROUND: Nuclear pleomorphism and tumor microenvironment (TME) play a critical role in cancer development and progression. Identifying most predictive nuclei and TME features of basal cell carcinoma (BCC) may provide insights into which characteristics pathologists can use to distinguish and stratify this entity. OBJECTIVES: To develop an automated workflow based on nuclei and TME features from basaloid cell tumor regions to differentiate BCC from trichoepithelioma (TE) and stratify BCC into high-risk (HR) and low-risk (LR) subtypes, and to identify the nuclear and TME characteristics profile of different basaloid cell tumors. METHODS: The deep learning systems were trained on 161 H&E -stained sections which contained 51 sections of HR-BCC, 50 sections of LR-BCC and 60 sections of TE from one institution (D1), and externally and independently validated on D2 (46 sections) and D3 (76 sections), from 2015 to 2022. 60%, 20% and 20% of D1 data were randomly splitted for training, validation and testing, respectively. The framework comprised four stages: tumor regions identification by multi-head self-attention (MSA) U-Net, nuclei segmentation by HoVer-Net, quantitative feature by handcrafted extraction, and differentiation and risk stratification classifier construction. Pixel accuracy, precision, recall, dice score, intersection over union (IoU) and area under the curve (AUC) were used to evaluate the performance of tumor segmentation model and classifiers. RESULTS: MSA-U-Net model detected tumor regions with 0.910 precision, 0.869 recall, 0.889 dice score and 0.800 IoU. The differentiation classifier achieved 0.977 ± 0.0159, 0.955 ± 0.0181, 0.885 ± 0.0237 AUC in D1, D2 and D3, respectively. The most discriminative features between BCC and TE contained Homogeneity, Elongation, T-T_meanEdgeLength, T-T_Nsubgraph, S-T_HarmonicCentrality, S-S_Degrees. The risk stratification model can well predict HR-BCC and LR-BCC with 0.920 ± 0.0579, 0.839 ± 0.0176, 0.825 ± 0.0153 AUC in D1, D2 and D3, respectively. The most discriminative features between HR-BCC and LR-BCC comprised IntensityMin, Solidity, T-T_minEdgeLength, T-T_Coreness, T-T_Degrees, T-T_Betweenness, S-T_Degrees. CONCLUSIONS: This framework hold potential for future use as a second opinion helping inform diagnosis of BCC, and identify nuclei and TME features related with malignancy and tumor risk stratification.

A Case of Uncommon S100-Negative CD1a-Positive Histiocytosis in a 9-Year-Old Boy: Clinical Presentation, Histopathologic Features, and Successful Treatment Approach.

ABSTRACT: Immunohistochemically, histiocytosis differentiating into Langerhans cells is typically characterized by the expression of CD1a, S100, and varying degrees of Langerin. However, CD1a-positive but S100-negative histiocytosis is extremely rare in clinical practice. We present a case of a 9-year-old boy with multiple erythematous to brown dome-shaped nodules. Histopathologic examination revealed dermal infiltrates of histiocytic cells, exhibiting a distinctive immunohistochemical profile of CD68+, S100-, CD1a+, and Langerin-. This exceptional case may contribute to our understanding of the etiology and differentiation processes of histiocytic proliferative disorders.

Mitochondrial dynamics disruption: Unraveling Dinotefuran's impact on cardiotoxicity.

Exposure to pesticides has been associated with several cardiovascular complications in animal models. Neonicotinoids are now the most widely used insecticide globally, while the impact of neonicotinoids on cardiovascular function and the role of mitochondrial dynamics in neonicotinoids-induced cardiotoxicity is unclear. In the present study, Xenopus laevis tadpoles were exposed to environmental related concentrations (0, 5, and 50 µg/L) of typical neonicotinoid dinotefuran, with two enantiomers, for 21 days. We evaluated the changes in heart rate and cardiomyocyte apoptosis in exposed tadpoles. Then, we performed the transcriptome, metabolomics, transmission electron microscopy (TEM), and protein immunoblot to investigate the potential adverse impact of two enantiomers of dinotefuran on cardiotoxicity associated with mitochondrial dynamics. We observed changes in heart rate and increased cardiomyocyte apoptosis in exposed tadpoles, indicating that dinotefuran had a cardiotoxic effect. We further found that the cardiac contractile function pathway was significantly enriched, while the glucose metabolism-related pathways were also disturbed significantly. TEM observation revealed that the mitochondrial morphology of cardiomyocytes in exposed tadpoles was swollen, and mitophagy was increased. Mitochondria fusion was excessively manifested in the enhanced mitochondrial fusion protein. The mitochondrial respiratory chain was also disturbed, which led to an increase in ROS production and a decrease in ATP content. Therefore, our results suggested that dinotefuran exposure can induce cardiac disease associated mitochondrial disorders by interfering with the functionality and dynamics of mitochondria. In addition, both two enantiomers of dinotefuran have certain toxicity to tadpole cardiomyocytes, while R-dinotefuran exhibited higher toxicity than S-enantiomer, which may be attributed to disparities in the activation capacities of the respiratory chain.

Refractory alopecia areata with single hairs imitating frontal fibrosing alopecia: a prospective observational study.

BACKGROUND: Lonely hair sign is considered as a clue to the diagnosis of frontal fibrosing alopecia (FFA). OBJECTIVE: To report an undescribed variant of alopecia areata (AA) with which the patient developed single hairs and other features similar to FFA and to determine the underlying mechanism. METHODS: We conducted a prospective observational study in patients who presented with receding hairline and single hairs, evaluating the clinical, trichoscopic, and histological features and their correlation. Immunochemistry studies were performed to describe the microenvironment. RESULTS: Eighteen patients were enrolled in the study. Despite the similarity to FFA clinically, these patients showed different histopathology which revealed a normal number of pilosebaceous units, one anagen hair in one or more pilosebaceous units, and others in telogen stage, consistent with single hairs under the naked eye or under trichoscopy. The severity of the hair loss assessed by SALT was no more than 50, but the response to conventional therapy was poor. CONCLUSIONS: This study reports a unique variant of AA. The pathological basis is an increase in the telogen hair follicles, with one anagen hair in one or more pilosebaceous units. Minimal inflammation consisting of CD3+ T lymphocytes and mast cells was demonstrated in the microenvironment.

The role and intervention of mitochondrial metabolism in osteoarthritis.

Osteoarthritis (OA), a prevalent degenerative joint disease, affects a substantial global population. Despite the elusive etiology of OA, recent investigations have implicated mitochondrial dysfunction as a significant factor in disease pathogenesis. Mitochondria, pivotal cellular organelles accountable for energy production, exert essential roles in cellular metabolism. Hence, mitochondrial dysfunction can exert broad-ranging effects on various cellular processes implicated in OA development. This comprehensive review aims to provide an overview of the metabolic alterations occurring in OA and elucidate the diverse mechanisms through which mitochondrial dysfunction can contribute to OA pathogenesis. These mechanisms encompass heightened oxidative stress and inflammation, perturbed chondrocyte metabolism, and compromised autophagy. Furthermore, this review will explore potential interventions targeting mitochondrial metabolism as means to impede or decelerate the progression of OA. In summary, this review offers a comprehensive understanding of the involvement of mitochondrial metabolism in OA and underscores prospective intervention strategies.

Epigenetic and transcription factors synergistically promote the high temperature response in plants.

Temperature is one of the main environmental cues affecting plant growth and development, and plants have evolved multiple mechanisms to sense and acclimate to high temperature. Emerging research has shown that transcription factors, epigenetic factors, and their coordination are essential for plant temperature responses and the resulting phenological adaptation. Here, we summarize recent advances in molecular and cellular mechanisms to understand how plants acclimate to high temperature and describe how plant meristems sense and integrate environmental signals. Furthermore, we lay out future directions for new technologies to reveal heterogeneous responses in different cell types thus improving plant environmental plasticity.

Gut microbiota dysbiosis involves in host non-alcoholic fatty liver disease upon pyrethroid pesticide exposure.

A growing body of evidence has demonstrated the significance of the gut microbiota in host health, while the association between gut microbiota dysbiosis and multiple diseases is yet elusive in the scenario of exposure to widely used pesticides. Here, we show that gut microbiota dysbiosis involves in host's abnormal lipid metabolism and consequently the non-alcoholic fatty liver disease in Xenopus laevis upon exposure to cis-bifenthrin, one of the most prevalent pyrethroid insecticides in the world. With the guidance of gut microbiota analysis, we found that cis-bifenthrin exposure significantly perturbed the gut microbial community, and the specific taxa that served as biomarkers were identified. Metabolomics profiling and association analysis further showed that a significant change of intestinal metabolites involved in lipid metabolic pathways were induced along with the microbiota dysbiosis upon exposure to cis-bifenthrin. Detailed investigation showed an altered functional regulation of lipids in the liver after cis-bifenthrin exposure and the accumulation of lipid droplets in hepatocytes. Specifically, a change in deoxycholic acid alters bile acid hepatoenteral circulation, which affects lipid metabolism in the liver and ultimately causes the development of fatty liver disease. Collectively, these findings provide novel insight into the gut microbiota dysbiosis upon pesticide exposure and their potential implication in the development of chronic host diseases related to liver metabolic syndrome.

First detection and complete genome analysis of porcine circovirus-like virus P1 and porcine circovirus-2 in yak in China.

Porcine circovirus-like virus P1, like porcine circovirus type 2 (PCV2), is a potential pathogen of post-weaning multisystemic wasting syndrome in swine. Yaks are a valuable species and an iconic symbol of the Tibet Plateau which is the highest and largest plateau in the world. In this study, a total of 105 yak diarrheal samples, collected from 13 farms in Linzhi in the Tibet Plateau from January 2019 to December 2021, that were screened for P1 and PCV2 by polymerase chain reaction, 10.48% (n = 11) were positive for P1, 4.76% (n = 5) for PCV2, and 5.71% (n = 6) were positive for coinfection of P1 and PCV2. In addition, the whole genomes of eight P1 strains and eight PCV2 strains were sequenced. Alignment of deduced amino acid sequences of P1 ORF1 and PCV2 ORF2 gene revealed that ON012566 had one unique amino acid mutation at residues 137 (T to P). This mutation has important implication for the study of virus virulence, tissue tropism, and immune response. Phylogenetic analysis shows that the yak-origin P1 strains in this study with cattle-origin P1 reference strains were grouped into one cluster. The yak-origin PCV2 (ON012566) and a buffalo-origin PCV2 (KM116514) reference strain clustered in the same branch in the PCV2b regions. Meanwhile, the remaining PCV2 strains and buffalo-origin PCV2 reference strain (ON012565) clustered in the PCV2d regions. To summarize, to our knowledge, this is the first report on the molecular prevalence and genome characteristics of P1 and PCV2 in yaks in the world and will contribute to further study of the molecular epidemiology, source, and evolution of P1 and PCV2 strains.

Decabromodiphenyl ethane induced hyperactivity in developing zebrafish at environmentally relevant concentrations.

Decabromodiphenyl ethane (DBDPE), a widely used novel brominated flame retardant, is gaining concerns due to rapidly increased contents in various environmental and biota samples. In the present study, zebrafish (Danio rerio) embryos were exposed to 2.91, 9.71, 29.14 and 97.12 µg/L of DBDPE until 120 h post-fertilization (hpf) to investigate the potential developmental neurotoxicity and underlying mechanisms. Chemical analysis revealed concentration-dependently increased body burdens of DBDPE in zebrafish larvae, with bioaccumulation factors (BCFs) ranging from 414 to 726. Embryonic exposure to DBDPE caused hyperactivity without affecting the development of secondary motoneuron axons and muscle fibers. However, further results implicated that DBDPE may affect the locomotor regulatory network via different mechanisms at lower and higher concentrations. On the one hand, embryonic exposure to 2.91 µg/L DBDPE transiently promoted spontaneous coiling contractions, but showed no effects on touch-response and swimming activity in zebrafish larvae. The whole-body contents of neurotransmitters were significantly decreased. Significant decreased protein abundances of α1-TUBULIN and SYN2a and molecular docking results pointed out possible interactions of DBDPE with these two proteins. However, these changes may be unconcerned with the transient hyperactivity, and the exact molecular mechanisms need further investigation. On the other hand, 29.14 and 97.12 µg/L DBDPE exposure caused longer-lasting effects in promoting spontaneous coiling contractions, and also touch-response and swimming activity. At the same time, increased ACh contents (without changes of other neurotransmitters) and ChAT activity and inhibited transcription of nAChRs were observed at higher concentrations. Molecular docking indicated direct interaction of DBDPE with ChAT. The results suggested that DBDPE induced hyperactivity at higher concentrations was probably involved with disrupted cholinergic system, with ChAT as a potential target. Given that the body burden of DBDPE in lower concentration group was comparable with those detected in wild fish, the current results may provide useful information for ecological risk assessment.

Porcine circovirus-like virus P1 activates pancreatic secretion pathway by interacting with CHRM3 protein.

The porcine circovirus-like virus P1, a member of the circovirus family, causes post-weaning multisystemic wasting syndrome (PMWS) in weaned piglets with progressive wasting as the main clinical symptom. The pancreatic secretion pathway induces pancreatic acinar cells to secrete various digestive enzymes and as such is an important signaling pathway for the digestive system and somatic growth. This study examined the effects and mechanism of P1 virus infection on the pancreatic secretion pathway. The experiment was conducted by transfecting double-copy plasmid P1 into PK-15 and 3D4 cells and by infecting cells with the P1 virus. Samples were collected at various times after transfection or infection. The pathway's transcription and translation levels of CHRM3, Gq, PLC-ß2, PRKCA, Rab3D, RhoA, Rac1, and amyA proteins were detected by real-time PCR and Western blots; these analyses confirmed that the P1 virus infection could upregulate the expression level of key pancreatic secretion signaling molecules. Then, we confirmed that the VP1 protein of the P1 virus could interact with the pathway initiation protein CHRM3 using Co-IP, pull-downs, and confocal fluorescence microscopy. Finally, we demonstrated that the VP1 protein activates the pancreatic secretory pathway through the CHRM3 protein. In conclusion, this study demonstrated that the P1 virus can interact with the CHRM3 receptor protein to activate the pancreatic secretion pathway and promote the secretion of various digestive enzymes downstream of the pathway, thereby providing a basis for P1 virus pathogenesis.

The histone H3K27 demethylase REF6/JMJ12 promotes thermomorphogenesis in Arabidopsis.

Dynamic trimethylation of histone H3 at Lys27 (H3K27me3) affects gene expression and controls plant development and environmental responses. In Arabidopsis thaliana, RELATIVE OF EARLY FLOWERING 6 (REF6)/JUMONJI DOMAIN-CONTAINING PROTEIN 12 demethylates H3K27me3 by recognizing a specific DNA motif. However, little is known about how REF6 activates target gene expression after recognition, especially in environmental responses. In response to warm ambient temperature, plants undergo thermomorphogenesis, which involves accelerated growth, early flowering and changes in morphology. Here we show that REF6 regulates thermomorphogenesis and cooperates with the transcription factor PHYTOCHROME INTERACTING FACTOR 4 to synergistically activate thermoresponsive genes under warm ambient temperature. The ref6 loss-of-function mutants exhibited attenuated hypocotyl elongation at warm temperature, partially due to downregulation of GIBBERELLIN 20-OXIDASE 2 and BASIC HELIX-LOOP-HELIX 87. REF6 enzymatic activity is necessary for warm ambient temperature responses. Together, our results provide direct evidence of an epigenetic modifier and a transcription factor working together to respond to the environment.

Nearly 20 Years of Genetic Diversity and Evolution of Porcine Circovirus-like Virus P1 from China.

Porcine circovirus-like virus P1 can infect many kinds of animals and mainly causes postweaning multisystemic wasting syndrome. In China, the genetic diversity, variation, and evolutionary processes of this virus have not been described yet. To improve our knowledge of its genetic diversity, evolution, and gene flow, we performed a bioinformatics analysis using the available nucleotide sequences of the P1 virus; among them, 12 nucleotide sequences were from ten pig farms in Jiangsu Province in this epidemiological survey, and 84 sequences were downloaded from GenBank. The P1 sequences showed a rich composition of AT nucleotides. Analyses of the complete genomic sequences were polymorphic and revealed high haplotype (gene) diversity and nucleotide diversity. A phylogenetic analysis based on the NJ method showed that all P1 virus sequences formed two distinct groups: A and B. High genetic differentiation was observed between strains from groups A and B. The codon usage pattern of P1 was affected by dinucleotide compositions. Dinucleotide UU/CC was overrepresented, and dinucleotide CG was underrepresented. The mean evolutionary rate of the P1 virus was estimated to be 3.64 × 10-4 nucleotide substitutions per site per year (subs/site/year). The neutrality tests showed negative values. The purifying selection and recombination events may play a major driving role in generating the genetic diversity of the P1 population. The information from this research may be helpful to obtain new insights into the evolution of P1.

HLA complex group 11 is involved in colorectal carcinoma cisplatin resistance via the miR-214-5p/SOX4 axis.

The aim of the present study was to investigate the roles and potential mechanisms of long non-coding RNA HLA complex group 11 (HCG11) in colorectal carcinoma. Reverse transcription-quantitative PCR was used to detect HCG11 expression in clinical tissues and survival analysis was performed to identify its prognostic value. In order to investigate its specific biological functions in colorectal carcinoma, the transfection technique was used for the knockdown and overexpression of HCG11. Dual-luciferase reporter gene and RNA pull-down assays were used to identify the binding association between HCG11 and microRNA (miR)-214-5p. Western blot analysis was used to detect the mechanism of epithelial-mesenchymal transition (EMT) regulation in tumor cells in the pathway downstream of HCG11. HCG11 level was high in colorectal carcinoma tissues, which was associated with poor patient prognosis; however, chemotherapy may prevent the upregulation of HCG11 in colorectal carcinoma. HCG11-knockdown suppressed the proliferation, migration and chemotherapeutic sensitivity of colorectal carcinoma cells, whereas HCG11-overexpression enhanced chemotherapeutic sensitivity. miR-214-5p was revealed to be a target gene, and upon direct interaction, a negative regulator of HCG11 in colorectal carcinoma cells. Inhibition of miR-214-5p reversed the restriction of HCG11 on the malignant activity of colorectal carcinoma cells, while miR-214-5p mediated the chemotherapy-related intracellular EMT pathway. In conclusion, HCG11 is a vital oncogene of colorectal carcinoma involved in mediating the chemotherapeutic resistance of tumors.

Interaction of porcine circovirus-like virus P1 capsid protein with host proteins.

BACKGROUND: Porcine circovirus-like virus P1 is a relatively new kind of virus that is closely related to the post-weaning multisystemic wasting syndrome, congenital tremors, and abortions in swine. The molecular mechanisms of P1 virus infection and pathogenesis are fully unknown. To analyze P1 and its host interactions, we used a yeast two-hybrid (Y2H) assay to identify cellular proteins interacting with the Cap of the P1 virus. In this study, the Cap of the P1 virus exhibited no self-activation and toxicity to yeast cells and was used as bait to screen the Y2H library prepared from the pancreas tissue. RESULTS: Five cellular proteins (EEP, Ral GDS, Bcl-2-L-12, CPS1, and one not identified) were found to interact with P1 Cap. The interaction between Cap and Ral GDS was confirmed by co-immunoprecipitation. CONCLUSIONS: Our data are likely to support the future investigation of the underlying mechanism of P1 infection and pathogenesis.

Nitrogen doped carbon spheres with wrinkled cages for the selective oxidation of 5-hydroxymethylfurfural to 5-formyl-2-furancarboxylic acid.

Nitrogen doped carbon spheres with wrinkled cages (NCSWCs), which were used for the first time as metal-free catalysts, exhibited high catalytic activity and selectivity in the oxidation of 5-hydroxymethylfurfural (HMF) to 5-formyl-2-furancarboxylic acid (FFCA) under base-free conditions using tert-butyl hydroperoxide (TBHP) as the oxidant. The mechanistic studies found that this reaction was catalyzed by the synergy between NCSWCs and TBHP. The density functional theory (DFT) calculations further suggested that the hydroperoxyl radicals from TBHP adsorbed on the carbon atoms adjacent to the graphitic N atoms are the active sites.

The combined adverse effects of cis-bifenthrin and graphene oxide on lipid homeostasis in Xenopus laevis.

Simultaneous exposure to multiple pollutants has received great concerns considering that the interactions between pollutants can alter the environment fate and bioavailability of pollutants with potentially deleterious effects. Graphene oxide (GO) has been widely used in many areas including environmental remediation, biology and agriculture. However, researchers have largely ignored the combined toxicity of GO with coexisting toxicants. Cis-bifenthrin (cis-BF), a typical synthetic pyrethroid insecticide, was frequently detected in the environment, which raised the possibility of interaction between cis-BF and GO. Our study investigated the toxic effects of cis-BF alone or combined with GO on the lipid homeostasis in Xenopus laevis. Tadpoles at 51 stage were exposed to cis-BF (0, 12, 60 and 300 ng/L) or in their combination with GO (0.1 mg/L) for 21 days. Coexposure to cis-BF and GO deteriorated the lipid homeostasis disruption in tadpoles. The up- or down-regulation of lipogenesis genes expression and enzymes activity were amplified in the coexposure groups. Furthermore, the presence of GO enhanced the deleterious impacts of cis-BF on the hepatic function in tadpoles. This study uniquely shows that GO promotes the lipotoxicity and hepatic function deficit caused by cis-BF exposure in frog.

Coexposure to environmental concentrations of cis-bifenthrin and graphene oxide: Adverse effects on the nervous system during metamorphic development of Xenopus laevis.

Despite the great concerns associated with the combined biological effects of nanoparticles and insecticides, the current understanding of the corresponding ecological risks remains limited. Xenopus laevis (X. laevis) tadpoles were exposed to various concentrations of typical pyrethroid (cis-bifenthrin; cis-BF), either alone or in combination with graphene oxide (GO), for 21 days. The presence of GO resulted in increased bioconcentration of cis-BF and a higher 1S-enantiomer fraction. Exposure to cis-BF and GO caused further reduction in pre-metamorphic developmental rates and activated dopaminergic, noradrenergic, and serotonergic neurotransmitter systems. Reduced tadpole activity and levels of genomic DNA methylation at cytosine nucleotides (5hmC) were observed in the coexposure groups. These results indicate that GO enhance the bioconcentration of cis-BF and promote the conversion of its 1R-enantiomer to the 1S form, which lead to disruption of neurotransmitter systems as well as interference in metamorphic development.

Exposure to graphene oxide at environmental concentrations induces thyroid endocrine disruption and lipid metabolic disturbance in Xenopus laevis.

Graphene oxide (GO) has become a topic of increasing concern for its environmental and health risks. However, the potential toxic effects of GO on wildlife remain limited. The present study chose the Xenopus laevis tadpole as a model to assess the thyroid endocrine disruption as well as the lipid metabolic disturbance of GO. Tadpoles at the 51 stage were exposed to GO (0, 0.01, 0.1, and 1 mg/L) for 21 days, when tadpoles were undergoing an extremely complicated phase of morphological changes and growth. GO treatment showed obvious developmental toxicity, such as shortened snout-to-vent length (SVL) and hind limb length (HLL), decreased body weight, and delayed developmental stage. Exposure to GO also induced obvious decreases in whole-body triiodothyronine (T3) and thyroxin (T4) concentrations. The mRNA expression of genes related to the hypothalamic-pituitary-thyroid (HPT) axis also changed significantly. Furthermore, we observed significant decline in the fatty acids and triglycerides (TGs) concomitantly with changes in the expression of genes involved in the synthesis and metabolism of lipids in GO exposure groups. In contrast, high-density lipoprotein (HDL) and total bile acid levels increased remarkably, but cholesterol and low-density lipoprotein (LDH) levels showed no obvious changes. Taken together, the results revealed for the first time that GO could induce thyroid endocrine disruption and produce obvious disturbance effect on lipid synthesis and metabolism.