Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chronic exposure to butyl-paraben causes photosensitivity disruption and memory impairment in adult zebrafish

ABSTRACT: Limited studies on neurotoxicity following chronic exposure to butyl-paraben (BuP) have been conducted. In this study, neurobehavior in zebrafish adults was assessed using a novel tank test, photomotor response tests, and T-maze tests after exposure to BuP for 28 days at the concentrations of 0, 0.01, 0.1, and 1.0 mg/L. To comprehensively understand the underlying molecular perturbations in the brain, alterations in transcripts, neurotransmitters, and neurosteroids were measured. We found that BuP penetrated the blood-brain barrier and impaired neurobehavior in photosensitivity at 1.0 mg/L and in memory at 0.1 and 1.0 mg/L. RNA-seq analysis showed that phototransduction, tight junctions, and neuroactive ligand receptor activity were significantly affected, which explains the observed abnormal neurobehaviors. Neurosteroid analysis revealed that BuP increased cortisol levels in a concentration-dependent manner and specifically reduced allopregnanolone levels at all tested concentrations, suggesting that cortisol and allopregnanolone are significant neurosteroid markers associated with photosensitivity and memory deficits. Collectively, we demonstrated that BuP can cross the blood-brain and modulates the levels of transcripts, associated with phototransduction and circadian rhythm, and neurosteroidal cortisol and allopregnanolone, resulting in abnormal neurobehavioral responses to light stimulation and learning and memory.

ORGANISM(S): Danio rerio

PROVIDER: GSE211530 | GEO | 2022/08/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Exposure of a bovine rumen microbiome model to glyphosate

Project description:We evaluated the effects of pure glyphosate and the formulations Durano TF and Roundup® LB plus in different concentrations on rumen microbiota bioreactor model using the Rumen Simulation Technique (RUSITEC). Application of the compounds in three concentrations (0.1 mg/L, 1.0 mg/L or 10 mg/L, n = 4 each).

2022-05-08 | PXD032166 | Pride

Chronic cortisol differentially impacts Major Depression-patient stem cell derived astrocytes in vitro

Project description:Major Depression (MDD) is a prevalent psychiatric disorder and exposure to stress is robust risk factor for MDD. Clinical data and rodent models have indicated the negative impact of chronic stress induced hormones like cortisol on brain volume, memory, and cell metabolism. However, the cellular and transcriptomic changes that occur in the brain after prolonged exposure to cortisol are less understood. Furthermore, astrocyte-specific contribution to cortisol-induced neuropathology remains understudied. Here, we have developed an in vitro model of “chronic stress” using human induced pluripotent stem cell-derived astrocytes treated with cortisol for 7 days. Whole transcriptome sequencing reveals differentially expressed genes (DEGs) uniquely regulated in chronic cortisol compared to acute cortisol treatment. Utilizing this paradigm, we examined the stress response transcriptome of astrocytes generated from MDD patient iPSCs. MDD-specific DEGs related to GPCR ligand binding, synaptic signaling, and ion homeostasis. Together, these data highlight the unique role astrocytes play in the central nervous system and present interesting genes for future study into the relationship between chronic stress and MDD.

2022-10-04 | GSE178071 | GEO

Cognitive Impairment in Colorectal Cancer Patients Receiving Cytotoxic Chemotherapy

Project description:The purpose of this research study is to see how the brain changes in patients receiving chemotherapy (cytotoxic drug) treatment for colon or rectal cancer at Parkview Cancer Institute. This information will be used to identify helpful tests to diagnose individuals at risk for developing difficulties with thinking and memory due to their cancer treatments.

| 2387341 | ecrin-mdr-crc

Effects of plasticizers on adult human adipocytes (SGBS) using global proteomics

Project description:SGBS cells were used as a model system to investigate the cellular mode of action of a variety of plasticizers in human adipocytes. In brief, cells were cultured at 5% CO2 and 37°C in 95% humidity. Cells of generation 40 and passage 3 after thawing were grown to confluence with DMEM/F12 containing 33 µM biotin, 17 µM pantothenate, 100 U/l penicillin, and 0.1 mg/l streptomycin (basal medium) supplemented with 10% FCS (Gibco, Carlsbad, CA, USA). According to the standard differentiation protocol, differentiation was initiated (day 0) after changing to serum-free basal medium supplemented with 0.1 μM cortisol, 0.01 mg/ml apo-transferrin, 0.2 nM triiodothyronine, and 20 nM human insulin (differentiation medium) with the addition of 2 µM rosiglitazone, 25 nM dexamethasone, and 200 µM 3-isobutyl-1-methylxanthine for the first four days. SGBS cells were first differentiated according to the standard protocol for 12 days. Obtained adult adipocytes were then exposed to the plasticizers for 8 days with medium changes every second day. The control contained equivalent amounts of solvent (0.01% MeOH). Additinally, a control on day 12 before exposure was sampled. All SGBS cell culture experiments were conducted in quadruplets.

2022-06-20 | PXD030843 | Pride

Project description:The hippocampus is especially susceptible to age-associated neuronal pathologies, and there is concern that the age-associated rise in cortisol secretion from the adrenal gland may contribute to their etiology. Furthermore, because 11β-hydroxysteroid dehydrogenase type 1 (HSD11B1) catalyzes the reduction of cortisone to the active hormone cortisol, it is plausible that an increase in the expression of this enzyme enhances the deleterious impact of cortisol in the hippocampus and contributes to the neuronal pathologies that underlie cognitive decline in the elderly. Rhesus macaques were used as a translational animal model of human aging, to examine age-related changes in gene and protein expressions of (HSD11B1/HSD11B1) in the hippocampus, a region of the brain that plays a crucial role in learning and memory. Older animals showed significantly (p<0.01) higher base-line cortisol levels in the circulation. In addition, they showed significantly (p<0.05) higher hippocampal expression of HSD11B1 but not NR3C1 and NR3C2 (i.e., two receptor-encoding genes through which cortisol exerts its physiological actions). A similar age-related significant (p<0.05) increase in the expression of the HSD11B1 was revealed at the protein level by Western blot analysis. The data suggest that an age-related increase in the expression of hippocampal HSD11B1 is likely to raise cortisol concentrations in this cognitive brain area, and thereby contribute to the etiology of neuropathologies that ultimately lead to neuronal loss and dementia. Targeting this enzyme pharmacologically may help to reduce the negative impact of elevated cortisol concentrations within glucocorticoid-sensitive brain areas and thereby afford neuronal protection.

2024-04-03 | GSE249907 | GEO

Skeletal muscle of glucocorticoid deprived and treated mice by SAGE

Project description:Forty male C57BL6 mice 12-15 weeks old fed chow ad libitum. 30 mice underwent adrenalectomy (Adx) and 10 others a sham-Adx. Three or 24 h before tissue sampling, groups of 10 mice received an I.P. injection of cortisol (0.1 mg per mice), while the remaining Adx and intact mice received an I.P. injection of the vehicle (ethanol) 24 h prior to the sacrifice. All mice were killed within a period of a few hours. Gastrocnemius muscle were dissected and pooled together for each one of the four groups. Total RNA was isolated by Trizol. Keywords: other

2005-01-06 | GSE2122 | GEO

Effect of Esketamine on Preventing Depression After Resection of the Colorectal Cancer: A Randomized Clinical Trial

Project description:Interventions: experimental group :Eesketamine + Sufentanil PCIA group (Group E, n=60, esketamine 1.0 mg / kg and sufentanil 2.0 µ g / kg);control group:Sufentanil PCIA group (Group C, n=60, sufentanil 2.0 µ g / kg) Primary outcome(s): HAMD grade;VAS grade;Postoperative adverse effects;Brain-derived neurotrophic factor(BDNF) Study Design: Parallel

| 106072 | ecrin-mdr-crc

Effects of plasticizers on human preadipocytes (SGBS) using global proteomics

Project description:SGBS cells were used as a model system to investigate the cellular mode of action of a variety of plasticizers in human adipocytes. In brief, cells were cultured at 5% CO2 and 37°C in 95% humidity. Cells of generation 40 and passage 3 after thawing were grown to confluence with DMEM/F12 containing 33 µM biotin, 17 µM pantothenate, 100 U/l penicillin, and 0.1 mg/l streptomycin (basal medium) supplemented with 10% FCS (Gibco, Carlsbad, CA, USA). According to the standard differentiation protocol, differentiation was initiated (day 0) after changing to serum-free basal medium supplemented with 0.1 μM cortisol, 0.01 mg/ml apo-transferrin, 0.2 nM triiodothyronine, and 20 nM human insulin (differentiation medium) with the addition of 2 µM rosiglitazone, 25 nM dexamethasone, and 200 µM 3-isobutyl-1-methylxanthine for the first four days. The positive control was differentiated using the standard protocol with rosiglitazone. For plasticizer treatments, differentiation was conducted without rosiglitazone and cells were continuously exposed from day 0 – day 16 to the plasticizers or their transformation products. As for plasticizer treatments, the negative control was differentiated with rosiglitazone-free medium containing equivalent amounts of solvent (0.01 MeOH, v/v) for 16 days, resulting in minimal differentiation. All media were renewed every second day to mimic continuous exposure.

2022-06-20 | PXD031041 | Pride

Skeletal muscle of glucocorticoid deprived and treated mice by SAGE

2005-01-05 | E-GEOD-2122 | biostudies-arrayexpress

Transcriptomic Evidence that Cortisol Alters Perinatal Epicardial Adipose Tissue Maturation

Project description:Cortisol administration during late gestation in ewes, modeling maternal stress, resulted in transcriptomic changes suggesting altered maturation and metabolic changes to the offspring heart. This study investigates the effects of cortisol on epicardial adipose tissue (EAT), a visceral fat pad associated with adverse cardiovascular conditions in adults. Pregnant ewes were treated with either 1 or 0.5 mg/kg/day cortisol from 115 days gestation to term and EAT collected from term fetuses (control: n=8, maternal cortisol 1 mg/kg/day: n=6) or two-week-old lambs (control: n=7, maternal cortisol 0.5mg/kg/day: n=9). Transcriptomic modeling was used to identify pathways altered by maternal cortisol over-exposure. Transcriptomic modeling confirmed the brown fat phenotype of EAT at term and a transition towards white fat at two weeks of age in EAT of control fetuses/lambs, and highlighted a role of immune responses, including complement-coagulation, and serotonin in this transition. Maternal cortisol (1mg/kg/day) increased the lipid peroxidation product 4-hydroxynonenal in EAT of term fetuses, but did not affect the number of activated macrophages or size of the lipid droplets in the depot; transcriptomics suggested an earlier metabolic maturation of EAT via, in part, increased immune responses. Conversely the transcriptomics in EAT of two-week-old lambs of ewes treated with a lower dose of cortisol (0.5mg/kg/day) suggested decreased metabolism of several substrates through both mitochondrial and cytosolic actions, and delayed maturation of EAT associated with a longer period of adipogenesis and angiogenesis.

2019-07-10 | GSE119254 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data