Effects of excessive iodine intake on brain development
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ABSTRACT:
PROVIDER: PRJNA1125318 | ENA |
REPOSITORIES: ENA
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Project description:To evaluate the impact of perinatal iodine excess intake on neurodevelopment, we conducted a gene expression profiling assessment using microarray technology. This evaluation was performed on the hippocampus of adult female offspring mice from both the 20-fold iodine intake group and the control group, which exhibited statistically significant differences in learning and memory-related behavioral experiments. Despite the observed behavioral differences, no significant differences were found in the gene expression profiles.
2025-06-01 | GSE270137 | GEO
Project description:Folate is crucial for diverse biological processes including neurogenesis. While folate supplementation during pregnancy is standard for preventing neural tube defects (NTDs), concerns are growing over the potential risks of excessive maternal intake. In this study, we employed spatial transcriptomics and single-nucleus multi-omics techniques to investigate the impact of increased maternal folate intake on offspring brain development. Elevated folate intake broadly affected gene pathways linked to neurogenesis and neuronal axon myelination across multiple brain regions. Furthermore, specific gene expression alterations related to learning and memory processes emerged in thalamic and ventricular regions. Single-nucleus multi-omics analysis revealed that maturing excitatory neurons in dentate gyrus are particularly vulnerable to suboptimal maternal folate intake. Aberrant gene expression and chromatin accessibility changes were primarily centered on pathways governing ribosomal biogenesis, which is critical for synaptic formation. Altogether, our findings provide novel insights into how excessive maternal folate supplementation affects offspring brain development, notably by influencing gene expression and chromatin accessibility.
2024-07-10 | GSE269543 | GEO
Project description:Folate is crucial for diverse biological processes including neurogenesis. While folate supplementation during pregnancy is standard for preventing neural tube defects (NTDs), concerns are growing over the potential risks of excessive maternal intake. In this study, we employed spatial transcriptomics and single-nucleus multi-omics techniques to investigate the impact of increased maternal folate intake on offspring brain development. Elevated folate intake broadly affected gene pathways linked to neurogenesis and neuronal axon myelination across multiple brain regions. Furthermore, specific gene expression alterations related to learning and memory processes emerged in thalamic and ventricular regions. Single-nucleus multi-omics analysis revealed that maturing excitatory neurons in dentate gyrus are particularly vulnerable to suboptimal maternal folate intake. Aberrant gene expression and chromatin accessibility changes were primarily centered on pathways governing ribosomal biogenesis, which is critical for synaptic formation. Altogether, our findings provide novel insights into how excessive maternal folate supplementation affects offspring brain development, notably by influencing gene expression and chromatin accessibility.
2024-07-10 | GSE269544 | GEO
Project description:Perchlorate, which is a ubiquitous and persistent ion, competitively interferes with iodide accumulation in the thyroid, causing iodine deficiency, which may result in reduced thyroid hormone synthesis and secretion. Human studies suggest that perchlorate presents very little risk in healthy individuals; however, the precautionary principle demands that the sensitive populations of iodine deficient adults and mothers require extra consideration. In an attempt to determine if the effects on gene expression were similar, we compared the thyroidal effects of perchlorate (10 mg/kg) treatment for 14 days in drinking water with those caused by 8 weeks of Iodine-deficiency in rats. The thyroids were collected (N=3 each group) and total mRNA was analyzed using the Affymetrix Rat Genome 230 2.0 GeneChip®. Changes in gene expression were compared with appropriate control groups. We compared the 2-fold gene changes due to I-deficiency with changes due to perchlorate treatment. 189 transcripts were changed by the Iodine-deficient diet and 722 transcripts were changed by the perchlorate treatment. 34% of the transcripts changed by the I-deficient diet were also changed by perchlorate and generally in the same direction. three specific transporter genes, AQP1, NIS, & SLC22A3 were changed by both treatments, indicating that the membrane specific changes were similar. Iodine-deficiency primarily caused changes in retinol and calcium signaling pathways and perchlorate primarily caused changes related to the accumulation of extracellular matrix proteins. This study provides evidence that perchlorate, at least at this dose level, changes more genes and changes different genes compared to iodine deficiency.
2010-11-04 | GSE25144 | GEO
Project description:Perchlorate, which is a ubiquitous and persistent ion, competitively interferes with iodide accumulation in the thyroid, causing iodine deficiency, which may result in reduced thyroid hormone synthesis and secretion. Human studies suggest that perchlorate presents very little risk in healthy individuals; however, the precautionary principle demands that the sensitive populations of iodine deficient adults and mothers require extra consideration. In an attempt to determine if the effects on gene expression were similar, we compared the thyroidal effects of perchlorate (10 mg/kg) treatment for 14 days in drinking water with those caused by 8 weeks of Iodine-deficiency in rats. The thyroids were collected (N=3 each group) and total mRNA was analyzed using the Affymetrix Rat Genome 230 2.0 GeneChip®. Changes in gene expression were compared with appropriate control groups. We compared the 2-fold gene changes due to I-deficiency with changes due to perchlorate treatment. 189 transcripts were changed by the Iodine-deficient diet and 722 transcripts were changed by the perchlorate treatment. 34% of the transcripts changed by the I-deficient diet were also changed by perchlorate and generally in the same direction. three specific transporter genes, AQP1, NIS, & SLC22A3 were changed by both treatments, indicating that the membrane specific changes were similar. Iodine-deficiency primarily caused changes in retinol and calcium signaling pathways and perchlorate primarily caused changes related to the accumulation of extracellular matrix proteins. This study provides evidence that perchlorate, at least at this dose level, changes more genes and changes different genes compared to iodine deficiency. Changes in gene expression due to I-deficiency compared to normal diet for 2 months. Changes in gene expression due to perchlorate in the drinking water compared to normal drinking water for 1 or 14 days. Feeding study in rats.
2010-11-04 | E-GEOD-25144 | biostudies-arrayexpress
Project description:The number and type of synthetic chemicals that are being produced worldwide continues to increase significantly. While these industrial chemicals provide numerous benefits, there is no doubt that some have potential to damage the environment and health. Toxicity must be evaluated and use must be carefully controlled and monitored in order to minimize potential damage. DNA microarray technology has become an important new technique in toxicology. We are using the yeast Saccharomyces cerevisiae as a model organism for toxicological study because it is a simple, fast-growing eukaryote that has been thoroughly characterized. In order to evaluate toxicity by newly synthesized or mixture chemicals, toxicity-induced gene expression alteration profiles by known chemicals should be collected. In our study, cells need to be exposed with same experimental cellular condition, semi lethal (IC50), respectively. In the case of iodine (CAS; 7553-56-2), the IC50 was 1 mM by growth curve with continuously diluted exposure. // Effects of Iodine on Global Gene Expression in Saccharomyces cerevisiae : It is well documented that iodine kills microorganisms with broad spectrum. However, a systematic study of its mechanism of action has not yet been reported. Here we have demonstrated the action of iodine on gene expression level, using the yeast Saccharomyces cerevisiae with a DNA microarray. It was found that like antimicrobial activity, iodine causes an immediate and dose-dependent (0.5 mM, 0.75 mM and 1 mM) transcriptional alteration on yeast cells. The effects of iodine continued after the first immediate response. Genes for C-compound and carbohydrate metabolism, for energy, and for cell rescue were continuously up-regulated. On the other hand, genes related to protein fate were induced especially at 0.5 h. The gene expression profile at 0.5 h was significantly different from other longer iodine exposed condition. The main reaction at 0.5 h after iodine addition may be due to the oxidative toxicity, and the profile at 0.5 h was similar to agricultural bactericide. Keywords: stress response
2007-11-01 | GSE9401 | GEO
Project description:In the present study, we investigated the consequences of trehalose intake on brain metabolism in mice drinking for 0, 1, and 10 days. Microarray analyses were performed to identify the molecular targets involved in the brain metabolism of trehalose intake.
2019-04-01 | GSE112976 | GEO
Project description:Iodine treatments specifically regulated the expression of several genes in shoot and root tissues, mostly involved in the plant defence response, suggesting the protective role of iodine against both biotic and abiotic stresses.
2021-01-01 | GSE157643 | GEO
Project description:Thyroid autonomy is a frequent cause of thyrotoxicosis in regions with iodine deficiency. Epidemiological data suggest that the prevalence of thyroid autonomy is not only inversely correlated with the ambient iodine supply, but that iodide may also influence the course of pre-existing thyroid autonomy with possibly different effects on thyroid growth and function. Iodine slows TSH effects on thyroid growth stimulation and this effect is more pronounced in thyrocytes with constitutive cAMP activation i.e. in thyroid autonomy. Iodine induced growth alteration in early stage thyroid autonomy is conferred by induction of apoptosis and G2/M arrest. Transcriptome analysis revealed significant modulation of gene networks relevant to cell adhesion, cadherin signalling and ion binding with more pronounced effects in constitutively active FRTL-5 cells compared to normal FRTL-5 cells.
2010-12-01 | GSE22118 | GEO
Project description:Thyroid autonomy is a frequent cause of thyrotoxicosis in regions with iodine deficiency. Epidemiological data suggest that the prevalence of thyroid autonomy is not only inversely correlated with the ambient iodine supply, but that iodide may also influence the course of pre-existing thyroid autonomy with possibly different effects on thyroid growth and function. Iodine slows TSH effects on thyroid growth stimulation and this effect is more pronounced in thyrocytes with constitutive cAMP activation i.e. in thyroid autonomy. Iodine induced growth alteration in early stage thyroid autonomy is conferred by induction of apoptosis and G2/M arrest. Transcriptome analysis revealed significant modulation of gene networks relevant to cell adhesion, cadherin signalling and ion binding with more pronounced effects in constitutively active FRTL-5 cells compared to normal FRTL-5 cells. The aim was to study iodide-induced changes in global gene expression in an in vitro model of thyroid autonomy. This model makes use of FRTL-5 cells with stable expression of a constitutively activating TSH receptor mutation or wild type TSHR as a control.
2010-12-01 | E-GEOD-22118 | biostudies-arrayexpress