Embryonic atrazine exposure elicits neuroendocrine dysfunction in adult male zebrafish
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PROVIDER: PRJNA293456 | ENA |
REPOSITORIES: ENA
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Project description:The developmental origins of health and adult disease (DOHaD) hypothesis states that exposure to various environmental stressors early in life can elicit changes to the genome and epigenome thereby resulting in an increased susceptibility of a disease state during adulthood. Atrazine, a common herbicide used throughout the Midwestern United States for control of weeds on various crops frequently contaminates potable water supplies and is a suspected endocrine disrupting chemical. Studies suggest atrazine elicits reproductive dysfunction through the hypothalamus-pituitary-gonadal (HPG) axis. In previous studies, zebrafish were exposed to 0.3, 3, or 30 parts per billion (ppb; ug/L) atrazine through embryogenesis, rinsed, and allowed to mature to adulthood. A decrease in spawning was observed in adults with an embryonic exposure. In addition, adult females had an increase in progesterone and ovarian follicular atresia, alterations in levels of a serotonin metabolite and serotonin turnover in brain tissue, and transcriptome alterations in brain and ovarian tissue supporting neuroendocrine alterations from an embryonic atrazine exposure were reported. Furthermore, offspring of the exposed population exhibited morphological alterations. As reproductive dysfunction may also be influenced by males, this study assessed transcriptomic profiles of brain and testes, morphology, histology, and hormone levels in adult males exposed to atrazine during embryogenesis. Transcriptomic profiles of adult male brain tissue revealed alterations in genes associated with cell to cell signaling and interaction of neurotransmission, cell morphology, cellular assembly and organization of neurites, cellular function and maintenance of neuritogenesis and synaptogenesis, and molecular transport of hormones. In addition, the transcriptomic profiles of adult male testes tissue demonstrated alterations in genes associated with lipid metabolism, molecular transport of steroids, small molecule biochemistry of lipids, and cell morphology. The embryonic atrazine exposure resulted in no alterations in body or testes weight, gonadosomatic index, testes histology, or levels of 11-ketotestosterone or testosterone in adult male zebrafish. Thus, although the transcriptomics data indicate later-in-life alterations on the neuroendocrine system of adult males exposed to atrazine during embryogenesis, analysis of additional endpoints is needed to determine functional impairments. We treated zebrafish embryos from approximately 1 hour post fertilization through 72 hours post fertilization (embryogenesis) to 0, 0.3, 3, or 30 parts per billion (ppb) atrazine. Following the 72 hour exposure period, larave were rinsed and allowed to mature under normal conditions until adulthood (5-6 months post fertilization). At this time, zebrafish were bred weekly for three weeks in order to initiate breeding cycles. Following this peroid, gonadal tissue was disseceted and processed for transcriptomic analysis.
2016-07-01 | E-GEOD-72243 | biostudies-arrayexpress
Project description:The developmental origins of health and adult disease (DOHaD) hypothesis states that exposure to various environmental stressors early in life can elicit changes to the genome and epigenome thereby resulting in an increased susceptibility of a disease state during adulthood. Atrazine, a common herbicide used throughout the Midwestern United States for control of weeds on various crops frequently contaminates potable water supplies and is a suspected endocrine disrupting chemical. Studies suggest atrazine elicits reproductive dysfunction through the hypothalamus-pituitary-gonadal (HPG) axis. In previous studies, zebrafish were exposed to 0.3, 3, or 30 parts per billion (ppb; ug/L) atrazine through embryogenesis, rinsed, and allowed to mature to adulthood. A decrease in spawning was observed in adults with an embryonic exposure. In addition, adult females had an increase in progesterone and ovarian follicular atresia, alterations in levels of a serotonin metabolite and serotonin turnover in brain tissue, and transcriptome alterations in brain and ovarian tissue supporting neuroendocrine alterations from an embryonic atrazine exposure were reported. Furthermore, offspring of the exposed population exhibited morphological alterations. As reproductive dysfunction may also be influenced by males, this study assessed transcriptomic profiles of brain and testes, morphology, histology, and hormone levels in adult males exposed to atrazine during embryogenesis. Transcriptomic profiles of adult male brain tissue revealed alterations in genes associated with cell to cell signaling and interaction of neurotransmission, cell morphology, cellular assembly and organization of neurites, cellular function and maintenance of neuritogenesis and synaptogenesis, and molecular transport of hormones. In addition, the transcriptomic profiles of adult male testes tissue demonstrated alterations in genes associated with lipid metabolism, molecular transport of steroids, small molecule biochemistry of lipids, and cell morphology. The embryonic atrazine exposure resulted in no alterations in body or testes weight, gonadosomatic index, testes histology, or levels of 11-ketotestosterone or testosterone in adult male zebrafish. Thus, although the transcriptomics data indicate later-in-life alterations on the neuroendocrine system of adult males exposed to atrazine during embryogenesis, analysis of additional endpoints is needed to determine functional impairments. We treated zebrafish embryos from approximately 1 hour post fertilization through 72 hours post fertilization (embryogenesis) to 0, 0.3, 3, or 30 parts per billion (ppb) atrazine. Following the 72 hour exposure period, larvae were rinsed and allowed to mature under normal conditions until adulthood (5-6 months post fertilization). At this time, zebrafish were bred weekly for three weeks in order to initiate breeding cycles. Following this peroid, gonadal tissue was dissected and processed for transcriptomic analysis.
2016-07-01 | E-GEOD-72242 | biostudies-arrayexpress
Project description:The developmental origins of health and adult disease (DOHaD) hypothesis states that exposure to various environmental stressors early in life can elicit changes to the genome and epigenome thereby resulting in an increased susceptibility of a disease state during adulthood. Atrazine, a common herbicide used throughout the Midwestern United States for control of weeds on various crops frequently contaminates potable water supplies and is a suspected endocrine disrupting chemical. Studies suggest atrazine elicits reproductive dysfunction through the hypothalamus-pituitary-gonadal (HPG) axis. In previous studies, zebrafish were exposed to 0.3, 3, or 30 parts per billion (ppb; ug/L) atrazine through embryogenesis, rinsed, and allowed to mature to adulthood. A decrease in spawning was observed in adults with an embryonic exposure. In addition, adult females had an increase in progesterone and ovarian follicular atresia, alterations in levels of a serotonin metabolite and serotonin turnover in brain tissue, and transcriptome alterations in brain and ovarian tissue supporting neuroendocrine alterations from an embryonic atrazine exposure were reported. Furthermore, offspring of the exposed population exhibited morphological alterations. As reproductive dysfunction may also be influenced by males, this study assessed transcriptomic profiles of brain and testes, morphology, histology, and hormone levels in adult males exposed to atrazine during embryogenesis. Transcriptomic profiles of adult male brain tissue revealed alterations in genes associated with cell to cell signaling and interaction of neurotransmission, cell morphology, cellular assembly and organization of neurites, cellular function and maintenance of neuritogenesis and synaptogenesis, and molecular transport of hormones. In addition, the transcriptomic profiles of adult male testes tissue demonstrated alterations in genes associated with lipid metabolism, molecular transport of steroids, small molecule biochemistry of lipids, and cell morphology. The embryonic atrazine exposure resulted in no alterations in body or testes weight, gonadosomatic index, testes histology, or levels of 11-ketotestosterone or testosterone in adult male zebrafish. Thus, although the transcriptomics data indicate later-in-life alterations on the neuroendocrine system of adult males exposed to atrazine during embryogenesis, analysis of additional endpoints is needed to determine functional impairments.
2016-07-01 | GSE72243 | GEO
Project description:The developmental origins of health and adult disease (DOHaD) hypothesis states that exposure to various environmental stressors early in life can elicit changes to the genome and epigenome thereby resulting in an increased susceptibility of a disease state during adulthood. Atrazine, a common herbicide used throughout the Midwestern United States for control of weeds on various crops frequently contaminates potable water supplies and is a suspected endocrine disrupting chemical. Studies suggest atrazine elicits reproductive dysfunction through the hypothalamus-pituitary-gonadal (HPG) axis. In previous studies, zebrafish were exposed to 0.3, 3, or 30 parts per billion (ppb; ug/L) atrazine through embryogenesis, rinsed, and allowed to mature to adulthood. A decrease in spawning was observed in adults with an embryonic exposure. In addition, adult females had an increase in progesterone and ovarian follicular atresia, alterations in levels of a serotonin metabolite and serotonin turnover in brain tissue, and transcriptome alterations in brain and ovarian tissue supporting neuroendocrine alterations from an embryonic atrazine exposure were reported. Furthermore, offspring of the exposed population exhibited morphological alterations. As reproductive dysfunction may also be influenced by males, this study assessed transcriptomic profiles of brain and testes, morphology, histology, and hormone levels in adult males exposed to atrazine during embryogenesis. Transcriptomic profiles of adult male brain tissue revealed alterations in genes associated with cell to cell signaling and interaction of neurotransmission, cell morphology, cellular assembly and organization of neurites, cellular function and maintenance of neuritogenesis and synaptogenesis, and molecular transport of hormones. In addition, the transcriptomic profiles of adult male testes tissue demonstrated alterations in genes associated with lipid metabolism, molecular transport of steroids, small molecule biochemistry of lipids, and cell morphology. The embryonic atrazine exposure resulted in no alterations in body or testes weight, gonadosomatic index, testes histology, or levels of 11-ketotestosterone or testosterone in adult male zebrafish. Thus, although the transcriptomics data indicate later-in-life alterations on the neuroendocrine system of adult males exposed to atrazine during embryogenesis, analysis of additional endpoints is needed to determine functional impairments.
2016-07-01 | GSE72242 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2016-07-01 | E-GEOD-72244 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-07-01 | GSE72244 | GEO
Project description:The herbicide atrazine, a suspected endocrine disrupting chemical (EDC), frequently contaminates potable water supplies. Studies suggest alterations in the neuroendocrine system along the hypothalamus-pituitary-gonadal axis; however, most studies address either developmental, pubertal, or adulthood exposures, with few investigations regarding a developmental origins hypothesis. In this study, zebrafish were exposed to 0, 0.3, 3, or 30 parts per billion (ppb) atrazine through embryogenesis and then allowed to mature with no additional chemical exposure. Reproductive function, histopathology, hormone levels, offspring morphology, and the ovarian transcriptome were assessed. Embryonic atrazine exposure resulted in a significant increase in progesterone levels in the 3 and 30 ppb groups. A significant decrease in spawning and a significant increase in follicular atresia in the 30 ppb group were observed. In offspring, a decrease in the head length to body ratio in the 30 ppb group, along with a significant increase in head width to body ratio in the 0.3 and 3 ppb groups occurred. Transcriptomic alterations involved genes associated with endocrine system development and function, tissue development, and behavior. This study provides evidence to support atrazine as an EDC causing reproductive dysfunction and molecular alterations in adults exposed only during embryogenesis and morphological alterations in their offspring. We treated zebrafish embryos from approximately 1 hour post fertilization through 72 hours post fertilization (embryogenesis) to 0, 0.3, 3, or 30 parts per billion atrazine. Following the 72 hour exposure period, larvae were rinsed and allowed to mature under normal conditions until adulthood (5-6 months post fertilization). At this time, zebrafish were bred weekly for three weeks in order to initiate breeding cycles. Following this peroid, gonadal tissue was dissected and processed for transcriptomic analysis.
2016-03-02 | E-GEOD-73740 | biostudies-arrayexpress
Project description:Atrazine is an agricultural herbicide used throughout the Midwestern United States that frequently contaminates potable water supplies resulting in human exposure. Using the zebrafish model system, an embryonic atrazine exposure was previously reported to decrease spawning rates with an increase in progesterone and ovarian follicular atresia in adult females. In addition, alterations in genes associated with distinct molecular pathways of the endocrine system were observed in brain and gonad tissue of the adult females and males. Current hypotheses for mechanistic changes in the developmental origins of health and disease include genetic (e.g., copy number alterations) or epigenetic (e.g., DNA methylation) mechanisms. As such, in the current study we investigated whether an atrazine exposure would generate copy number alterations (CNAs) in the zebrafish genome. A zebrafish fibroblast cell line was used to limit detection to CNAs caused by the chemical exposure. First, cells were exposed to a range of atrazine concentrations and a crystal violet assay was completed, showing confluency decreased by ~60% at 46.3 µM. Cells were then exposed to 0, 0.463, 4.63, or 46.3 µM atrazine and array comparative genomic hybridization completed. Results showed 34, 21, and 44 CNAs in the 0.463, 4.63, and 46.3µM treatments, respectively. Furthermore, CNAs were associated with previously reported gene expression alterations in adult male and female zebrafish. This study demonstrates that atrazine exposure can generate CNAs that are linked to gene expression alterations observed in adult zebrafish exposed to atrazine during embryogenesis providing a mechanism of the developmental origins of atrazine endocrine disruption.
2017-02-20 | GSE93635 | GEO
Project description:The herbicide atrazine, a suspected endocrine disrupting chemical (EDC), frequently contaminates potable water supplies. Studies suggest alterations in the neuroendocrine system along the hypothalamus-pituitary-gonadal axis; however, most studies address either developmental, pubertal, or adulthood exposures, with few investigations regarding a developmental origins hypothesis. In this study, zebrafish were exposed to 0, 0.3, 3, or 30 parts per billion (ppb) atrazine through embryogenesis and then allowed to mature with no additional chemical exposure. Reproductive function, histopathology, hormone levels, offspring morphology, and the ovarian transcriptome were assessed. Embryonic atrazine exposure resulted in a significant increase in progesterone levels in the 3 and 30 ppb groups. A significant decrease in spawning and a significant increase in follicular atresia in the 30 ppb group were observed. In offspring, a decrease in the head length to body ratio in the 30 ppb group, along with a significant increase in head width to body ratio in the 0.3 and 3 ppb groups occurred. Transcriptomic alterations involved genes associated with endocrine system development and function, tissue development, and behavior. This study provides evidence to support atrazine as an EDC causing reproductive dysfunction and molecular alterations in adults exposed only during embryogenesis and morphological alterations in their offspring.
2016-03-02 | GSE73740 | GEO
Project description:The developmental origins of health and disease (DOHaD) hypothesis states that exposure to environmental stressors early in life can elicit genome and epigenome changes resulting in an increased susceptibility of a disease state during adulthood. Atrazine, a common agricultural herbicide used throughout the Midwestern United States, frequently contaminates potable water supplies and is a suspected endocrine disrupting chemical. In our previous studies, zebrafish was exposed to 0, 0.3, 3, or 30 parts per billion (?g/l) atrazine through embryogenesis, rinsed, and allowed to mature to adulthood. A decrease in spawning was observed with morphological alterations in offspring. In addition, adult females displayed an increase in ovarian progesterone and follicular atresia, alterations in levels of a serotonin metabolite and serotonin turnover in brain tissue, and transcriptome changes in brain and ovarian tissue supporting neuroendocrine alterations. As reproductive dysfunction is also influenced by males, this study assessed testes histology, hormone levels, and transcriptomic profiles of testes and brain tissue in the adult males. The embryonic atrazine exposure resulted in no alterations in body or testes weight, gonadosomatic index, testes histology, or levels of 11-ketotestosterone or testosterone. To further investigate potential alterations, transcriptomic profiles of adult male testes and brain tissue was completed. This analysis demonstrated alterations in genes associated with abnormal cell and neuronal growth and morphology; molecular transport, quantity, and production of steroid hormones; and neurotransmission with an emphasis on the hypothalamus-pituitary-adrenal and hypothalamus-pituitary-thyroid axes. Overall, this data indicate future studies should focus on additional neuroendocrine endpoints to determine potential functional impairments.
| S-EPMC5013880 | biostudies-other