Correction: Histopathologic Alterations Associated with Global Gene Expression Due to Chronic Dietary TCDD Exposure in Juvenile Zebrafish
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PROVIDER: S-EPMC4143344 | biostudies-literature | 2014 Jan
REPOSITORIES: biostudies-literature
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Project description:The goal of this project was to investigate the effects and possible developmental disease implication of chronic dietary TCDD exposure on global gene expression anchored to histopathologic analysis in juvenile zebrafish by functional genomic, histopathologic and analytic chemistry methods. Specifically, juvenile zebrafish were fed Biodiet starter with TCDD added at 0, 0.1, 1, 10 and 100 ppb, and fish were sampled following 0, 7, 14, 28 and 42 d after initiation of the exposure. TCDD accumulated in a dose- and time-dependent manner and 100 ppb TCDD caused TCDD accumulation in female (15.49 ppb) and male (18.04 ppb) fish at 28 d post exposure. Dietary TCDD caused multiple lesions in liver, kidney, intestine and ovary of zebrafish and functional dysregulation such as depletion of glycogen in liver, retrobulbar edema, degeneration of nasal neurosensory epithelium, underdevelopment of intestine, and diminution in the fraction of ovarian follicles containing vitellogenic oocytes. Importantly, lesions in nasal epithelium and evidence of endocrine disruption based on alternatively spliced vasa transcripts are two novel and significant results of this study. Microarray gene expression analysis comparing vehicle control to dietary TCDD revealed dysregulated genes involved in pathways associated with cardiac necrosis/cell death, cardiac fibrosis, renal necrosis/cell death and liver necrosis/cell death. These baseline toxicological effects provide evidence for the potential mechanisms of developmental dysfunctions induced by TCDD and vasa as a biomarker for ovarian developmental disruption.
| S-EPMC4079602 | biostudies-literature
Project description:The goal of this project was to use functional genomic methods to identify molecular biomarkers as indicators of the impact of TCDD exposure in rainbow trout. Specifically, we investigated the effects of chronic dietary TCDD exposure on whole juvenile rainbow trout global gene expression associated with histopathological analysis. Juvenile rainbow trout were fed Biodiet starter with TCDD added at 0, 0.1, 1, 10 and 100 ppb (ngTCDD/g food), and fish were sampled from each group at 7, 14, 28 and 42 days after initiation of feeding. 100 ppb TCDD caused 100% mortality at 39 days. Fish fed with 100 ppb TCDD food had TCDD accumulation of 47.37 ppb (ngTCDD/g fish) in whole fish at 28 days. Histological analysis from TCDD-treated trout sampled from 28 and 42 days revealed that obvious lesions were found in skin, oropharynx, liver, gas bladder, intestine, pancreas, nose and kidney. In addition, TCDD caused anemia in peripheral blood, decreases in abdominal fat, increases of remodeling of fin rays, edema in pericardium and retrobulbar hemorrhage in the 100 ppb TCDD-treated rainbow trout compared to the control group at 28 days. Dose- and time-dependent global gene expression analyses were performed using the cGRASP 16,000 (16K) cDNA microarray. TCDD-responsive whole body transcripts identified in the microarray experiments have putative functions involved in various biological processes including growth, cell proliferation, metabolic process, and immune system processes. Nine microarray-identified genes were selected for QPCR validation. CYP1A3 and CYP1A1 were common up-regulated genes and HBB1 was a common down-regulated gene among each group based on microarray data, and their QPCR validations are consistent with microarray data for the 10 and 100 ppb TCDD treatment groups after 28 days exposure (p<0.05). In addition, in the 100 ppb group at 28 days, expression of complement component C3-1 and trypsin-1 precursor have a more than 10-fold induction from the microarray experiments, and their QPCR validations are consistent and showed significant induction in the 100 ppb group at 28 days (p<0.05). Overall, lesion in nasal epithelium is a novel and significant result in this study, and TCDD-responsive rainbow trout transcripts identified in the present study may lead to the development of new molecular biomarkers for assessing the potential impacts of environmental TCDD on rainbow trout populations.
| S-EPMC3791104 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2014-12-01 | GSE47549 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2013-04-05 | GSE45781 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-04-05 | E-GEOD-45781 | biostudies-arrayexpress
Project description:Juvenile zebrafish were fed Biodiet starter (4% body weight per day) for 42 d with TCDD added at 0 ppb, 0.1 ppb, 1 ppb, 10 ppb or 100 ppb. Fish were collected, sexed, weighed and length measured at 0, 7, 14, 28 or 42 d for TCDD assessment, histopathologic and microarray analysis. Microarray experiments were conducted using 0 and 100 ppb-TCDD treated male and female sexed zebrafish at 7, 14, 28 and 42 d. NimbleGen Gene Expression 12X135K zebrafish microarrays and One-Color DNA labeling Kit (NimbleGen, WI) were used for genome-wide expression analysis of TCDD-treated zebrafish. TCDD accumulated in a dose- and time-dependent manner and 100 ppb TCDD caused TCDD accumulation in female (15.49 ppb) and male (18.04 ppb) fish at 28 d post exposure. TCDD caused multiple lesions in liver, kidney, intestine and ovary of zebrafish and functional dysregulation such as depletion of glycogen in liver, retrobulbar edema, degeneration of neurosensory epithelium, underdevelopment of intestine, and diminution in the fraction of ovarian follicles containing vitellogenic oocytes. At 42d, no mature female fish were observed.
2014-12-01 | GSE47547 | GEO
Project description:Juvenile zebrafish were fed Biodiet starter (4% body weight per day) for 42 d with TCDD added at 0 ppb, 0.1 ppb, 1 ppb, 10 ppb or 100 ppb. Fish were collected, sexed, weighed and length measured at 0, 7, 14, 28 or 42 d for TCDD assessment, histopathologic and microarray analysis. Microarray experiments were conducted in TCDD-treated (at 0, 0.1, 1, 10 and 100 ppb) for male and female sexed zebrafish at 28 d. NimbleGen Gene Expression 12X135K zebrafish microarrays and One-Color DNA labeling Kit (NimbleGen, WI) were used for genome-wide expression analysis of TCDD-treated zebrafish. TCDD accumulated in a dose- and time-dependent manner and 100 ppb TCDD caused TCDD accumulation in female (15.49 ppb) and male (18.04 ppb) fish at 28 d post exposure. TCDD caused multiple lesions in liver, kidney, intestine and ovary of zebrafish and functional dysregulation such as depletion of glycogen in liver, retrobulbar edema, degeneration of neurosensory epithelium, underdevelopment of intestine, and diminution in the fraction of ovarian follicles containing vitellogenic oocytes. Microarray gene expression analysis comparing control to post TCDD diet revealed dysregulated genes located in pathways associated with cardiac necrosis/cell death, cardiac fibrosis, renal necrosis/cell death and liver necrosis/cell death. These baseline toxicological effects provide evidence for the potential biomarkers, mechanisms and pathology of TCDD induced dysregulation.
2014-12-01 | GSE47434 | GEO
Project description:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), the classic aryl hydrocarbon receptor (AhR) agonist, is a potent environmental toxicant and endocrine-disrupting chemical (EDC) with known developmental toxicity in humans, rodents, and fish. Early life exposure to some EDCs, including TCDD, is linked to the occurrence of adult-onset and multigenerational disease. Previous work exposing juvenile F0 zebrafish (Danio rerio) to 50 ppt (parts per trillion) TCDD during reproductive development has shown male-mediated transgenerational decreases in fertility (F0-F2) and histologic and transcriptomic alterations in F0 testes. Here, we analyzed male germline alterations in F1 and F2 adult fish, looking for changes in testicular histology and gene expression inherited through the male lineage that could account for decreased reproductive capacity. Testes of TCDD-lineage F1 fish displayed an increase in spermatogonia (immature germ cells) and decrease in spermatozoa (mature germ cells). No histological changes were present in F2 fish. Transcriptomic analysis of exposed F1 and F2 testes revealed alterations in lipid and glucose metabolism, oxidation, xenobiotic response, and sperm cell development and maintenance genes, all of which are implicated in fertility outcomes. Overall, we found that differential expression of reproductive genes and reduced capacity of sperm cells to mature could account for the reproductive defects previously seen in TCDD-exposed male zebrafish and their descendants, providing insight into the distinct multigenerational effects of toxicant exposure.
| S-EPMC6061693 | biostudies-literature
Project description:Toxic effects of dietary TCDD on juvenile zebrafish
| PRJNA206051 | ENA
Project description:We investigated the effects of chronic TCDD exposure on global gene expression in developing rainbow trout (Oncorhynchus mykiss). Juvenile rainbow trout(0.18±0.01g) were fed Biodiet starter with TCDD added at 0, 0.1, 1, 10 and 100ppb, and ten fish were sampled and pooled from 10 ppb group at 7, 14, 28 and 42 days for microarray experiments after initiation of the exposure. Gene expression analysis was performed using the Genomics Research on All Salmonids Project (cGRASP) 16K cDNA microarrays. TCDD-responsive whole body transcripts identified in the microarray experiments have putative functions involved in various biological processes including response to stimulus, cell wall organization or biogenesis, growth and cell proliferation. In addition, TCDD caused leisons in multiple organ systems in juvenile rainbow, including skin, oropharynx, liver, gas bladder, intestine, pancreas, nose and kidney.
2013-04-05 | GSE45780 | GEO