Could changes in sphingolipid metabolism/transcriptome reflect neurotoxicity of environmental pollutants?

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00027162%3A_____%2F19%3AN0000281" target="_blank" >RIV/00027162:_____/19:N0000281 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Could changes in sphingolipid metabolism/transcriptome reflect neurotoxicity of environmental pollutants?

Popis výsledku v původním jazyce

FEBS - Sphingolipid Biology: Sphingolipids in Physiology and Pathology, 6.-10.5.2019, Cascais, Portugal – poster. Persistent organic pollutants are routinely spread over the large areas worldwide and accumulation of their levels in our environment represent one of the major health safety problem as degradation rate of these compounds is generally rather low and occurs in range of decades. Byproducts generated during industrial manufacturing (e.g. dioxins) as well as intentionally produced industrial chemicals (e.g. polychlorinated biphenyls) are known carcinogens and neurotoxic chemicals. However, mechanisms of their action leading to neurotoxicity are poorly characterized. We used 2,3,7,8tetrachlorodibenzopdioxin (TCDD) and 2,2´,4,4´,5,5´hexachlorobiphenyl (PCB153) as prototypical persistent toxicants for establishment of in vitro models suitable for testing neurotoxicity. In the first part of study, we employed undifferentiated murine neuroectodermal NE4C cells and human neuroblastoma SKNSH cells and exposed them for 24h to tested compounds. Our preliminary data show changes in sphingolipid (SL) metabolism after TCDD treatment, especially at the levels of hexosylceramide, sphingosine and dihydrosphingosine. Besides, we monitored expression levels of genes, which protein products are involved in sphingolipid metabolism using custom PCR array of 120 human genes of SL and cholesterol metabolism. In the second part of study, we simulated neurogenesis using retinoic acid (RA)induced differentiation of NE4C cells chronically exposed to TCDD, PCB153 or vehicle (DMSO) in order to describe changes in SL metabolism. Compilation of data from undifferentiated cells and their differentiated progeny may help to better understand whether changes in SL metabolism induced by toxic stress in undifferentiated neural cells could reflect and predict defects in their differentiated progeny during chemically disrupted neurogenesis.

Název v anglickém jazyce

Could changes in sphingolipid metabolism/transcriptome reflect neurotoxicity of environmental pollutants?

Popis výsledku anglicky

FEBS - Sphingolipid Biology: Sphingolipids in Physiology and Pathology, 6.-10.5.2019, Cascais, Portugal – poster. Persistent organic pollutants are routinely spread over the large areas worldwide and accumulation of their levels in our environment represent one of the major health safety problem as degradation rate of these compounds is generally rather low and occurs in range of decades. Byproducts generated during industrial manufacturing (e.g. dioxins) as well as intentionally produced industrial chemicals (e.g. polychlorinated biphenyls) are known carcinogens and neurotoxic chemicals. However, mechanisms of their action leading to neurotoxicity are poorly characterized. We used 2,3,7,8tetrachlorodibenzopdioxin (TCDD) and 2,2´,4,4´,5,5´hexachlorobiphenyl (PCB153) as prototypical persistent toxicants for establishment of in vitro models suitable for testing neurotoxicity. In the first part of study, we employed undifferentiated murine neuroectodermal NE4C cells and human neuroblastoma SKNSH cells and exposed them for 24h to tested compounds. Our preliminary data show changes in sphingolipid (SL) metabolism after TCDD treatment, especially at the levels of hexosylceramide, sphingosine and dihydrosphingosine. Besides, we monitored expression levels of genes, which protein products are involved in sphingolipid metabolism using custom PCR array of 120 human genes of SL and cholesterol metabolism. In the second part of study, we simulated neurogenesis using retinoic acid (RA)induced differentiation of NE4C cells chronically exposed to TCDD, PCB153 or vehicle (DMSO) in order to describe changes in SL metabolism. Compilation of data from undifferentiated cells and their differentiated progeny may help to better understand whether changes in SL metabolism induced by toxic stress in undifferentiated neural cells could reflect and predict defects in their differentiated progeny during chemically disrupted neurogenesis.

Druh

O - Ostatní výsledky

CEP obor

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OECD FORD obor

10601 - Cell biology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů