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Bing Zhang

Publications and source records attributed to Bing Zhang.

At least 19 recordsLinked to original sources
PubMed2026

Proteogenomic analysis of pediatric and AYA high-grade glioma reveals age-dependent biology, female-male differences, and kinase targets.

High-grade gliomas (HGGs) in children and adolescents and young adults (AYA) exhibit distinct biology across the neurodevelopmental spectrum. To dissect tumor-intrinsic molecular characteristics independent of developmental variation, we perform comprehensive proteogenomic analyses of tumors from 112 HGG patients aged 0-40 years. Our multi-omics analysis identifies two AYA subgroups-adolescents (aged 15-26 years) and young adults (aged 26-40 years)-with distinct molecular profiles and survival outcomes. Tumor-normal comparisons and survival modeling highlight roles of oxidative phosphorylation and neuronal system biology in glioma progression. Causal network analysis and cell line studies provide a rationale for personalized therapies targeting candidate kinases, such as CDK8. Survival modeling, clustering, and immune-landscape analyses identify proteins, post-translational modifications, and immune signatures linked to outcomes and reveal clinically relevant differences between male and female patients.

adolescent and young adult glioma↗
PubMed2026

AI proteomics: from protein identification to virtual cells.

Artificial intelligence (AI) is transforming scientific research, including proteomics. In this Perspective, we highlight key mass spectrometry (MS)-based proteomics areas where AI is driving innovation, ranging from protein identification to building AI virtual cells. These include improving peptide and protein identification and quantification; characterizing protein-protein interactions and protein complexes; advancing spatial and perturbation proteomics; integrating multi-omics data; and, ultimately, enabling AI virtual cells. Finally, we call for global collaboration among data producers, data consumers and other stakeholders to establish an AI-friendly ecosystem for MS-based proteomics, laying the foundation for transformative advancements in proteomics driven by AI.

Proteomics↗
PubMed2026

Source- and Solubility-specific Choline, Gut Microbiota, and Dyslipidemia Risk: Trimethylamine N-oxide-associated and Non-trimethylamine N-oxide-Associated Patterns in a Prospective Cohort Study.

BACKGROUND: Dietary choline, a major precursor of the gut microbial metabolite trimethylamine N-oxide (TMAO), is implicated in dyslipidemia risk; however, source- and form-specific associations and interactions with gut microbiota remain unclear. OBJECTIVES: The aim of this study was to examine longitudinal associations of source- and form-specific dietary choline with plasma TMAO and dyslipidemia and to identify gut microbiota interactions. METHODS: Using data from the China Health and Nutrition Survey (2018-2023), dietary intake was assessed via 3 consecutive 24-h recalls in this prospective cohort study. Two-level generalized linear mixed-effects models were applied in 4828 adults (mean age: 55.9 ± 12.6 y, 56.6% females) to assess choline-dyslipidemia associations. Choline-TMAO and TMAO-dyslipidemia analyses were conducted in 1091 participants free of dyslipidemia at baseline. Among 7169 adults with gut microbiome data, Least Absolute Selection and Shrinkage Operator and logistic regression identified lipid-associated gut genera; TMAO relationships were examined in a subset of 693 participants. RESULTS: Higher intakes of total [Q4 compared with Q1: odds ratio (OR) = 1.261; 95% confidence interval (CI): 1.007, 1.580], red meat-derived (OR: 1.753; 95% CI: 1.196, 2.568), and lipid-soluble choline (OR: 1.304; 95% CI: 1.047, 1.624) were associated with higher risk of elevated low-density lipoprotein cholesterol (LDL cholesterol), whereas vegetable-derived choline was inversely associated. Egg-derived and lipid-soluble choline were positively associated with plasma TMAO, which was prospectively associated with 5-y incident dyslipidemia (Q4 compared with Q1-OR: 1.620; 95% CI: 1.047, 2.509), elevated LDL cholesterol (Q3 compared with Q1-OR: 2.478; 95% CI: 1.187, 5.174), and hypertriglyceridemia (Q4 compared with Q1-OR: 1.829; 95% CI: 1.028, 3.225). Three TMAO-associated genera were identified: Lachnospiraceae and Phascolarctobacterium as pro-risk taxa and Turicibacter as protective. The adverse LDLcholesterol association of egg-derived choline was observed exclusively in Phascolarctobacterium-enriched individuals. CONCLUSIONS: Dietary choline source and solubility differentially associated with dyslipidemia risk through TMAO-associated and non-TMAO-associated patterns, with gut microbiota as key modulators.

Humans↗
PubMed2026

Enhanced HIF-1α cooperation by a human RORγt mutant potentiates Th17 pathogenicity.

T helper 17 (Th17) cells are pivotal in mucosal defense and autoimmune pathology, with their function governed by the transcription factor retinoic acid receptor-related orphan receptor gamma t (RORγt). Although genome-wide association studies link RORC variants to inflammatory diseases, their functional consequences remain poorly understood. We identify a pathogenic RORγt mutation N277D (mouse homolog N275D) that amplifies Th17 pathogenicity through cooperation with hypoxia-inducible factor HIF-1α. This mutation enhances IFN-γ and other Th1-type cytokine production by Th17 cells, exacerbating colitis without disrupting T cell development or homeostasis. Integrated transcriptomic and metabolomic profiling reveals activation of glycolytic and hypoxia-associated pathways, consistent with increased RORγtN275D recruitment by HIF-1α to the Pdk1 locus. Notably, silencing Pdk1 normalizes the excessive IFN-γ production in RORγtN275D Th17 cells. Together, these findings define a regulatory axis linking RORγt and HIF-1α that coordinates transcriptional and metabolic programs in pathogenic Th17 cells, providing a framework for dissecting the functional impact of autoimmune risk variants.

CP: immunology↗
PubMed2026

mRNA therapy: A novel approach for retinal neurodegenerative diseases.

Retinal neurodegeneration remains a major cause of irreversible vision loss, yet current therapeutic options are limited in effectiveness. Although gene therapies have shown clinical potential, the overexpression platforms they rely on, such as adeno-associated virus DNA, are constrained by safety concerns, limited efficacy, and cargo size restrictions. In contrast, mRNA therapy has gained recognition as a compelling alternative, enabling rapid and efficient protein expression without the risk of genomic integration. This review synthesizes recent advances in mRNA engineering, delivery systems, and administration routes for retinal applications, and highlight strategies to enhance targeting, penetration, and controlled release through interdisciplinary collaboration between ophthalmology and bioengineering. In recent years, engineered mRNA formats, including chemically modified linear, circular, and self-amplifying RNA, can achieve higher translation efficiency within a tunable expression window. The transient nature and relatively low immunogenicity of in vitro transcribed mRNA support repeat dosing without insertional mutagenesis. Advances in nanocarriers, particularly lipid nanoparticles, have enabled preferential delivery to retinal neurons, Müller glia, and pigment epithelium via intraocular administration, while improving mRNA stability and transfection efficiency. In preclinical studies, mRNA has been widely used to deliver gene-editing tools, transcription factors, and supplementary functional proteins. In disease models such as optic nerve crush and laser-induced choroidal neovascularization, mRNA-based therapies enhance neuroprotection and suppress pathological angiogenesis in the injured retina, with favorable ocular safety profiles. However, it remains largely unexplored how the intrinsic advantages of mRNA therapy can be leveraged to develop tailored strategies for complex retinal disorders. Consistent with this gap, mRNA platforms have not yet been widely incorporated into retinal research or clinical practice. In parallel, clinical translation also lags: despite encouraging outcomes of lipid nanoparticle-mRNA formulations in preclinical models, no candidates have progressed into retinal clinical trials. This review draws on the complex pathology and therapeutic logic of retinal neurodegeneration. It proposes that mRNA therapy enables multitarget, repeatable, stage-specific interventions that align with the dynamic evolution of diseases and the requirements of combination therapy in retinal diseases. It may be used to support neuroprotection, axon regeneration, and neurovascular regulation. By integrating data across experimental models and modalities, this review outlines representative cases and experimental paradigms to guide rational trial design and carrier selection. Taken together, technical progress and evolving application strategies position mRNA therapy as a compelling therapeutic avenue for retinal neurodegeneration.

administration↗
PubMed2026

CTRP9 ameliorates heart failure with preserved ejection fraction by regulating lipid metabolism.

BACKGROUND: Heart failure with preserved ejection fraction (HFpEF) is a major clinical challenge, with cardiac lipotoxicity emerging as a key driver of disease progression. Despite CTRP9’s role in lipid metabolism and cardioprotective properties, its therapeutic potential in HFpEF remains unexplored. This study aimed to investigate whether CTRP9 ameliorates HFpEF by regulating cardiac lipid metabolism and to identify the underlying molecular mechanisms. METHODS: In the established two-hit HFpEF mouse model (induced by a high-fat diet and L-NAME), the mice were treated with either CTRP9 or saline. Cardiac function was evaluated by echocardiography, while hypertrophy, fibrosis, and lipid accumulation were assessed using histology and molecular assays. Proteomic sequencing was further employed to identify downstream targets of CTRP9. RESULTS: CTRP9 treatment significantly improved diastolic function and attenuated cardiac hypertrophy and fibrosis in HFpEF mice. Myocardial lipid accumulation was substantially reduced, accompanied by enhanced fatty acid oxidation. Proteomic analysis identified GPD1 as a key downstream target upregulated by CTRP9. Cardiac-specific knockdown of GPD1 partly abolished the therapeutic benefits of CTRP9. CONCLUSION: Our data suggest that CTRP9 ameliorates HFpEF through GPD1-mediated regulation of cardiac lipid metabolism, identifying the CTRP9-GPD1 axis as a promising therapeutic target for HFpEF.

Animals↗
PubMed2025

Rat somatic genome editing enables ER+ breast cancer modeling.

Genetically engineered mouse models have advanced cancer research but often fail to capture key features of certain human tumors. Rats, with distinct physiology and tumor biology, offer a powerful alternative, yet their use has been constrained by technical barriers to genome editing. Here, we report efficient somatic genome editing in rats, enabling both Indel and substitution mutations. We then apply this approach to model estrogen receptor (ER)-positive breast cancer, which accounts for ~70% of human cases but remains poorly represented in mice. The resulting rat tumors reproduce hallmarks of human ER+ breast cancer, including ductal histology, hormone responsiveness, and immune-microenvironmental features. By contrast, identical genetic alterations in mice failed to yield ER+ tumors, underscoring critical species differences in tumorigenesis. Together, this work establishes a versatile platform for rapid generation of clinically relevant rat tumor models, opening new avenues to dissect tumor biology, therapeutic response, and immune interactions in previously inaccessible cancer subtypes.

Journal Article↗
PubMed2006

Residue-free sodium phosphate tablets (OsmoPrep) versus Visicol for colon cleansing: a randomized, investigator-blinded trial.

BACKGROUND: The bowel purgative Visicol contains microcrystalline cellulose (MCC) residue, which may impair full visibility during a colonoscopy. An MCC residue-free sodium phosphate (RF-NaP; OsmoPrep) tablet was developed. OBJECTIVE: To investigate appropriate RF-NaP dosing. DESIGN: Phase 2, randomized, investigator-blinded study. SETTING: Six research centers in the United States. PATIENTS AND INTERVENTIONS: Patients undergoing a colonoscopy received Visicol (n = 34) or 1 of 6 RF-NaP regimens administered as either split (S) dosing (the evening before and the day of colonoscopy) or evening-only (E) dosing. Dosing regimens for RF-NaP were 40 tablets S, 3 every 15 minutes (n = 33); 40 tablets S, 4 every 15 minutes (n = 34); 32 tablets E, 4 every 15 minutes (n = 34); 32 tablets S, 4 every 15 minutes (n = 36); 28 tablets E, 4 every 15 minutes (n = 34); 28 tablets S, 4 every 15 minutes (n = 34). Visicol was administered as 40 tablets S, 3 every 15 minutes. MAIN OUTCOME MEASURE: Overall colon cleansing (OCC) was assessed by a physician questionnaire (4-point scale, based on colonic contents). An OCC rating of "excellent" or "good" was considered a response. Safety measures were also monitored. RESULTS: Split dosing with RF-NaP was associated with high OCC and achieved response rates of 90%, 97%, and 100% for 28, 32, and 40 tablets, respectively, compared with 86% for Visicol. In addition, RF-NaP evening-only regimen response rates were 90% (32 tablets) and 72% (28 tablets). Transient shifts in electrolyte levels were reduced, and GI adverse events were less common with lower RF-NaP dose regimens. CONCLUSIONS: Administration of RF-NaP retains the benefits of a tablet purgative but eliminates MCC issues. Split dosing and 32-tablet evening-only dosing of RF-NaP tablets were efficacious and well tolerated, and split dosing of RF-NaP tablets is recommended.

Adolescent↗
PubMed2006

Adenovirus-mediated expression of both antisense ornithine decarboxylase and s-adenosylmethionine decarboxylase induces G1 arrest in HT-29 cells.

To evaluated the effect of recombinant adenovirus Ad-ODC-AdoMetDCas which can simultaneously express both antisense ornithine decarboxylase (ODC) and Sadenosylmethionine decarboxylase (AdoMetDC) on cell cycle distribution in colorectal cancer cell and investigated underlying regulatory responses, human colorectal cancer cells HT-29 were cultured in RPMI 1640 medium and infected with Ad-ODC-AdoMetDCas. Cell cycle progression was detected by flow cytometry analysis. The expression levels of cell cycle regulated proteins were measured by Western blot analysis. The mRNA level of cyclin D1 was measured by RT-PCR. And a luciferase reporter plasmid of cyclin D1 promoter was constructed to observe the effect of Ad-ODC-AdoMetDCas on cyclin D1 promoter activity. The results showed that recombinant adenovirus Ad-ODC-AdoMetDCas significantly induced G1 arrest, decreased levels of cyclin D1 protein and mRNA and suppressed the promoter activity. Ad-ODC-AdoMetDCas also inhibited nuclear translocation of beta-catenin. In conclusion, downregulation of ODC and AdoMetDC mediated by Ad-ODC-AdoMetDCas transfection induces G(1) arrest in HT-29 cells and the arrest was associated with suppression of cyclin D1 expression and inhibition of beta-catenin nuclear translocation. As a new anticancer reagent, the recombinant adenovirus Ad-ODC-AdoMetDCas holds promising hope for the therapy of colorectal cancers.

Adenosylmethionine Decarboxylase↗
PubMed2006

Br(2Pj) atom formation dynamics in ultraviolet photodissociation of tert-butyl bromide and iso-butyl bromide.

The photodissociation dynamics of tert-C(4)H(9)Br and iso-C(4)H(9)Br has been studied at 234 and 265 nm using two-dimensional velocity map imaging technique. The translational energy and angular distributions have been analyzed for Br, Br(*), and tert-C(4)H(9) radical. The energy distribution of Br atom in the photodissociation of tert-C(4)H(9)Br is found to consist of two Gaussian components. The two components are correlated to two independent reaction paths on the excited potential energy surfaces: (1) the high-energy component from the prompt dissociation along the C-Br stretching mode and (2) the low-energy component from the repulsive mode along the C-Br stretching, coupled with some bending motions. For the energy distribution of Br(*) atom in the photodissociation of tert-C(4)H(9)Br, a third multiphoton dissociative ionization channel is observed at 265 nm in addition to the two energy components corresponding to channels (1) and (2). The energy distributions of Br and Br(*) atoms in the photodissociation of iso-C(4)H(9)Br can be fitted using only one Gaussian function indicating a single formation channel. Relative quantum yields for Br((2)P(32)) at 234 and 265 nm in the photodissociation of tert-C(4)H(9)Br are measured to be 0.76 and 0.65, respectively. For iso-C(4)H(9)Br, the measured value is Phi(234 nm)(Br)=0.81. The contribution of bending modes to Br and Br(*) is much more obvious in the photodissociation of tert-C(4)H(9)Br than in iso-C(4)H(9)Br.

Journal Article↗
PubMed2006

Photodissociation dynamics of allyl bromide at 234, 265, and 267 nm.

The photodissociation dynamics of allyl bromide was investigated at 234, 265, and 267 nm. A two-dimensional photofragment ion velocity imaging technique coupled with a [2+1] resonance-enhanced multiphoton ionization scheme was utilized to obtain the angular and translational energy distributions of the nascent Br* (2P1/2) and Br (2P3/2) atoms. The Br fragments show a bimodal translational energy distribution, while the Br* fragments reveal one translational energy distribution. The vertical excited energies and the mixed electronic character of excited states were calculated at ab initio configuration interaction method. It is presumed that the high kinetic energy bromine atoms are attributed to the predissociation from 1(pipi*) or 1(pisigma*) state to the repulsive 1(nsigma*) state, and to the direct dissociation from 3(nsigma*) and 3(pisigma*) states, while the low kinetic energy bromine atoms stem from internal conversion from the lowest 3(pipi*) state to 3(pisigma*) state.

Journal Article↗
PubMed2006

Molecular dynamics simulations on the inhibition of cyclin-dependent kinases 2 and 5 in the presence of activators.

Interests in CDK2 and CDK5 have stemmed mainly from their association with cancer and neuronal migration or differentiation related diseases and the need to design selective inhibitors for these kinases. Molecular dynamics (MD) simulations have not only become a viable approach to drug design because of advances in computer technology but are increasingly an integral part of drug discovery processes. It is common in MD simulations of inhibitor/CDK complexes to exclude the activator of the CDKs in the structural models to keep computational time tractable. In this paper, we present simulation results of CDK2 and CDK5 with roscovitine using models with and without their activators (cyclinA and p25). While p25 was found to induce slight changes in CDK5, the calculations support that cyclinA leads to significant conformational changes near the active site of CDK2. This suggests that detailed and structure-based inhibitor design targeted at these CDKs should employ activator-included models of the kinases. Comparisons between P/CDK2/cyclinA/roscovitine and CDK5/p25/roscovitine complexes reveal differences in the conformations of the glutamine around the active sites, which may be exploited to find highly selective inhibitors with respect to CDK2 and CDK5.

Cyclin-Dependent Kinase 2↗
PubMed2006

Safety and colon-cleansing efficacy of a new residue-free formulation of sodium phosphate tablets.

OBJECTIVE: A residue-free sodium phosphate tablet (RF-NaP) was formulated that lacks microcrystalline cellulose, which can appear as a whitish residue in the colon. A multicenter, randomized, investigator-blinded study was conducted to compare the colon-cleansing efficacy of 40 or 32 tablets of RF-NaP with the marketed 40-tablet NaP treatment regimen. METHODS: Eight hundred sixteen patients were randomized prior to colonoscopy to receive either 40 tablets (60 g) of NaP or RF-NaP or 32 tablets (48 g) of RF-NaP. Colon cleansing was assessed using a 4-point scale based on retained "colonic contents." The primary end point was overall colon-cleansing response rate to treatment (score of excellent/good) versus nonresponse (fair/inadequate). RESULTS: Seven hundred four patients were included in the efficacy analysis. The overall colon-cleansing response rates were comparable among treatment arms (94.5%, 97.0%, and 95.3% for NaP, RF-NaP 40, and RF-NaP 32 tablets, respectively). Ascending colon-cleansing response rates for RF-NaP 40 (95.7%) and 32 tablets (93.6%) were significantly better than for NaP tablets (88.5%, p < 0.03 for both). Patients treated with RF-NaP 32 tablets experienced less pronounced changes in electrolyte levels and fewer adverse events (138/239, 58%) compared with patients receiving NaP (161/238, 68%, p= 0.07) and RF-NaP 40 tablets (156/236, 66%, p= 0.03). The most common adverse events reported were abdominal distention, nausea, abdominal pain, and vomiting. CONCLUSIONS: Based on the safety, efficacy, and patient preferences, the 32-tablet RF-NaP regimen was superior to the 40-tablet RF-NaP and NaP regimen for colon cleansing prior to colonoscopy.

Adolescent↗
PubMed2006

Transcriptome analysis of Deinagkistrodon acutus venomous gland focusing on cellular structure and functional aspects using expressed sequence tags.

BACKGROUND: The snake venom gland is a specialized organ, which synthesizes and secretes the complex and abundant toxin proteins. Though gene expression in the snake venom gland has been extensively studied, the focus has been on the components of the venom. As far as the molecular mechanism of toxin secretion and metabolism is concerned, we still knew a little. Therefore, a fundamental question being arisen is what genes are expressed in the snake venom glands besides many toxin components? RESULTS: To examine extensively the transcripts expressed in the venom gland of Deinagkistrodon acutus and unveil the potential of its products on cellular structure and functional aspects, we generated 8696 expressed sequence tags (ESTs) from a non-normalized cDNA library. All ESTs were clustered into 3416 clusters, of which 40.16% of total ESTs belong to recognized toxin-coding sequences; 39.85% are similar to cellular transcripts; and 20.00% have no significant similarity to any known sequences. By analyzing cellular functional transcripts, we found high expression of some venom related genes and gland-specific genes, such as calglandulin EF-hand protein gene and protein disulfide isomerase gene. The transcripts of creatine kinase and NADH dehydrogenase were also identified at high level. Moreover, abundant cellular structural proteins similar to mammalian muscle tissues were also identified. The phylogenetic analysis of two snake venom toxin families of group III metalloproteinase and serine protease in suborder Colubroidea showed an early single recruitment event in the viperids evolutionary process. CONCLUSION: Gene cataloguing and profiling of the venom gland of Deinagkistrodon acutus is an essential requisite to provide molecular reagents for functional genomic studies needed for elucidating mechanisms of action of toxins and surveying physiological events taking place in the very specialized secretory tissue. So this study provides a first global view of the genetic programs for the venom gland of Deinagkistrodon acutus described so far and an insight into molecular mechanism of toxin secreting.

Animals↗
PubMed2006

Study of the inhibition of cyclin-dependent kinases with roscovitine and indirubin-3'-oxime from molecular dynamics simulations.

Molecular dynamics simulations were performed to elucidate the interactions of CDK2 and CDK5 complexes with three inhibitors: R-roscovitine, S-roscovitine, and indirubin-3'-oxime. The preference of the two complexes for R-roscovitine over the S enantiomer, as reported by the experiment, was also found by the simulations. More importantly, the simulations showed that the cause of the stronger affinity for the R enantiomer is the presence of an important hydrogen bond between R-roscovitine and the kinases not found with S-roscovitine. The simulations also showed two amino acid mutations in the active site of CDK5/R-roscovitine that favor binding-enhanced electrostatic contributions, making the inhibitor more effective for CDK5 than for CDK2. This suggests that the effectiveness of roscovitine-like inhibitors can be improved by enhancing their electrostatic interaction with the kinases. Finally, molecular mechanics-Possion-Boltzmann/surface area calculations of the CDK5/indirubin-3'-oxime system in both water-excluded and water-included environments gave significantly different electrostatic contributions to the binding. The simulations detected the displacement of a water molecule in the active site of the water-included CDK/indirubin-3'-oxime system. This resulted in a more conserved binding pattern than the water-excluded structure. Hence, in the design of new indirubin-like inhibitors, it is important to include the water molecule in the analysis.

Binding Sites↗
PubMed2006

Polymorphisms in DNA repair genes and risk of non-Hodgkin lymphoma among women in Connecticut.

Several hereditary syndromes characterized by defective DNA repair are associated with high risk of non-Hodgkin lymphoma (NHL). To explore whether common polymorphisms in DNA repair genes affect risk of NHL in the general population, we evaluated the association between single nucleotide polymorphisms (SNPs) in DNA repair genes and risk of NHL in a population-based case-control study among women in Connecticut. A total of 518 NHL cases and 597 controls recruited into the study provided a biologic sample. Thirty-two SNPs in 18 genes involved in several DNA repair pathways were genotyped. Genotype data were analyzed by unconditional logistic regression adjusting for age and race. SNPs in four genes (ERCC5, ERCC2, WRN, and BRCA1) were associated with altered risk of NHL and diffuse large B-cell lymphoma (DLBCL), the major B cell subtype. In particular, ERCC5 Asp1104His was associated with increased risk of NHL overall (OR: 1.46; 95% CI: 1.13-1.88; P=0.004), DLBCL (OR: 1.44; 95% CI: 0.99-2.09; P=0.058), and also T cell lymphoma. WRN Cys1367Arg was associated with decreased risk of NHL overall (OR: 0.71; 95% CI: 0.56-0.91; P=0.007) and DLBCL (OR: 0.66; 95% CI: 0.45-0.95; P=0.024), as well as follicular and marginal zone lymphomas. Genetic polymorphisms in DNA repair genes, particularly ERCC5 and WRN, may play a role in the pathogenesis of NHL, especially for DLBCL. Further work is needed to extend these findings by carrying out extended haplotype analyses of these and related genes and to replicate the observations in other studies.

Adult↗
PubMed2006

Evidence for the transfer of polychlorinated biphenyls, polychlorinated dibenzo-p-dioxins, and polychlorinated dibenzofurans from soil into biota.

The concentrations of six indicator and co-planar polychlorinated biphenyls (PCBs), 17 polychlorinated dibenzo-p-dioxins, and polychlorinated dibenzofurans (PCDD/Fs) were determined in soil and associated biota samples collected from a polluted and wasted farmland in southern China. The sum of six indicator PCBs (Nos 28, 52, 101, 138, 153 and 180) concentrations in biota samples were proportional to the total amount of PCBs that transferred from soil to the corresponding biota samples, and the sum six indicator PCB congeners in samples were about 20% of the total PCBs, respectively. The ratios of the sum six indicator PCBs and the total PCBs in samples collected in the same area were approximately equal. The sums of six indicator PCBs were proportional to the total PCBs that transferred from soil to plant, while the co-planar PCBs were not. Analysis of individual PCB and PCDD/F congener signatures in soil revealed the original pollutant source after transportation and biodegradation for 14 years using principal component analysis (PCA). The pattern of PCBs in soils and plants could reflect the original pollution source after transportation and biodegradation for 14 years, while the pattern of PCBs in the terrestrial animals could not reflect the primary source. The consumption foods in this region such as foraging chicken eggs, foraging duck eggs, and loach (Misgurnus anguillicaudatus) were highly contaminated, the total toxicity equivalent (TEQ) was up to 784 pg WHO-TEQ/g on basis lipid in foraging chicken eggs.

Animals↗