Cadmium chloride-induced gene expression changes in D. melanogaster
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ABSTRACT:
PROVIDER: PRJNA485974 | ENA |
REPOSITORIES: ENA
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Project description:Heavy metals and organic compounds, such as pesticides and plasticizers, exert toxicity through their ability to perturb molecular mechanisms. We investigated the ability of 18 compounds to modify the epigenetic state of the white locus in a Drosophila model of position-effect variegation (PEV). Our data indicate that cadmium chloride (CdCl2) is a potent enhancers of variegation. We demonstrate that genes differentially expressed upon CdCl2 exposure are enriched for genes that have heterochromatic states associated with them.
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Project description:This is a study to explore the transcriptional changes after cadmium treatment in adult rat testes at three time points (control--0 hour, 8 hour and 4 day). Cadmium is an environmental toxicant that is known to affect the male reproductive system. It disrupts the blood-testis barrier irreversibly, and affects the Sertoli-germ cells adhesion, causing germ cell depletion from the seminiferous epithelium. Experiment Overall Design: Adult Sprague-Dawley rats treated with a single dose of cadmium chloride at 3 mg/kg b.w. by i.p. and terminated after 8 hours (n=2) and 20 hours (n=2). Testes from cadmium-treated rats and untreated (control, 0 hour, n=3) rats were harvested and total RNA were prepared. Standard Affymetrix genechip procedures were followed for the subsequent experiments. Data were analysed in MAS 5.0 and GeneSpring 7.2.
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Project description:We performed microarray-based expression profiling on liver of male zebrafish exposed to 30 µg/L of cadmium (II) chloride for 8-96 h, to identify global transcriptional programs and biological pathways involved in cadmium-induced adaptive responses under in vivo environment.
2013-12-31 | GSE41623 | GEO
Project description:We performed microarray-based expression profiling on liver of female zebrafish exposed to 30 µg/L of cadmium (II) chloride for 8-96 h, to identify global transcriptional programs and biological pathways involved in cadmium-induced adaptive responses under in vivo environment.
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Project description:Cadmium is a natural element that can accumulate to toxic levels in the environment leading to detrimental effects in animals and humans including kidney, liver and lung injuries. Using a transcriptomics approach, genes and cellular pathways affected by a low dose of cadmium were investigated. Adult largemouth bass were intraperitoneally injected with 20 µg/kg of cadmium chloride and microarray analyses were conducted in the liver and testis 48 hours after injection. Transcriptomics profiles identified in response to cadmium treatment were tissue-specific with the most differential expression changes found in the liver tissues, which also contained much higher levels of cadmium than the testes. Acute exposure to a low dose of cadmium induced oxidative stress response and oxidative damage pathways in the liver. The mRNA levels of antioxidants such as catalase increased and numerous transcripts related to DNA damage and DNA repair were significantly altered. Hepatic mRNA levels of metallothionein, a proposed marker of cadmium exposure, showed a small insignificant increase after 48 hours exposure. Carbohydrate metabolic pathways were also disrupted in cadmium-exposed fish with hepatic transcripts such as UDP-glucose pyrophosphorylase 2 and sorbitol dehydrogenase highly induced. Both tissues exhibited a disruption of steroid signalling pathways. In the testis, estrogen receptor beta and transcripts linked to cholesterol metabolism were suppressed. On the contrary, genes involved in cholesterol metabolism were highly increased in the liver including genes encoding for the rate limiting steroidogenic acute regulatory protein and the catalytic enzyme 7-dehydrocholesterol reductase. Integration of the transcriptomics data using functional enrichment analyses revealed a number of enriched gene networks associated with previously reported adverse outcomes of cadmium exposure such as liver toxicity and impaired reproduction. Adult largemouth bass (n=4 per treatment) were ip injected with a single dose of cadmium chloride (20 ug/kg) or a saline solution. After 48 hours, liver and testis were excised and differential gene expression profiles were examined.
2014-04-02 | E-GEOD-53047 | biostudies-arrayexpress
Project description:We performed microarray-based expression profiling on liver of female zebrafish exposed to 30 µg/L of cadmium (II) chloride for 8-96 h, to identify global transcriptional programs and biological pathways involved in cadmium-induced adaptive responses under in vivo environment. We analyzed 10 arrays of Cadmium-treated adult female zebrafish liver and 12 arrays of control fish.
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Project description:We performed microarray-based expression profiling on liver of male zebrafish exposed to 30 µg/L of cadmium (II) chloride for 8-96 h, to identify global transcriptional programs and biological pathways involved in cadmium-induced adaptive responses under in vivo environment. We analyzed 10 arrays of Cadmium-treated adult male zebrafish liver and 12 arrays of control fish.
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Project description:Cadmium is an environmental pollutant that has extensive deleterious effects. However, the mechanisms underlying the hepatotoxicity induced by long-term exposure to cadmium remained undefined. In the present study, we explored the role of m6A methylation in the development of cadmium-induced liver disease. We showed a dynamic change of RNA methylation in liver tissue from mice administrated with cadmium chloride (CdCl2) for 3, 6 and 9 months, respectively. Particularly, the METTL3 expression was declined in a time-dependent manner, associated with the degree of liver injury, indicating the involvement of METTL3 in hepatotoxicity induced by CdCl2. Moreover, we established a mouse model with liver-specific over-expression of Mettl3 and administrated these mice with CdCl2 for 6 months. Notably, METTL3 highly expressed in hepatocytes attenuated CdCl2-induced steatosis and liver fibrosis in mice. In vitro assay also showed METTL3 overexpression ameliorated the CdCl2-induced cytotoxicity and activation of primary hepatic stellate cells. Furthermore, transcriptome analysis identified 268 differentially expressed genes both in mice liver tissue treated with CdCl2 for 3 months and 9 months. Among them, 115 genes were predicted to be regulated by METTL3 determined by m6A2Target database. Further analysis revealed the perturbation of metabolic pathway, glycerophospholipid metabolism, ErbB signaling pathway, Hippo signaling pathway, and choline metabolism in cancer, and circadian rhythm, led to hepatotoxicity induced by CdCl2. Collectively, our findings reveal new insight into the crucial role of epigenetic modifications in hepatic diseases caused by long-term exposure to cadmium.
2023-06-30 | GSE230188 | GEO
Project description:Cadmium is a natural element that can accumulate to toxic levels in the environment leading to detrimental effects in animals and humans including kidney, liver and lung injuries. Using a transcriptomics approach, genes and cellular pathways affected by a low dose of cadmium were investigated. Adult largemouth bass were intraperitoneally injected with 20 µg/kg of cadmium chloride and microarray analyses were conducted in the liver and testis 48 hours after injection. Transcriptomics profiles identified in response to cadmium treatment were tissue-specific with the most differential expression changes found in the liver tissues, which also contained much higher levels of cadmium than the testes. Acute exposure to a low dose of cadmium induced oxidative stress response and oxidative damage pathways in the liver. The mRNA levels of antioxidants such as catalase increased and numerous transcripts related to DNA damage and DNA repair were significantly altered. Hepatic mRNA levels of metallothionein, a proposed marker of cadmium exposure, showed a small insignificant increase after 48 hours exposure. Carbohydrate metabolic pathways were also disrupted in cadmium-exposed fish with hepatic transcripts such as UDP-glucose pyrophosphorylase 2 and sorbitol dehydrogenase highly induced. Both tissues exhibited a disruption of steroid signalling pathways. In the testis, estrogen receptor beta and transcripts linked to cholesterol metabolism were suppressed. On the contrary, genes involved in cholesterol metabolism were highly increased in the liver including genes encoding for the rate limiting steroidogenic acute regulatory protein and the catalytic enzyme 7-dehydrocholesterol reductase. Integration of the transcriptomics data using functional enrichment analyses revealed a number of enriched gene networks associated with previously reported adverse outcomes of cadmium exposure such as liver toxicity and impaired reproduction.
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