Mitochondrial damage precedes the changes of glutathione metabolism in CdCl2 treated neuronal SH-SY5Y cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216275%3A25310%2F24%3A39921750" target="_blank" >RIV/00216275:25310/24:39921750 - isvavai.cz</a>

Výsledek na webu

<a href="https://www.sciencedirect.com/science/article/abs/pii/S0278691524005192?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/abs/pii/S0278691524005192?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.fct.2024.114953" target="_blank" >10.1016/j.fct.2024.114953</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Mitochondrial damage precedes the changes of glutathione metabolism in CdCl2 treated neuronal SH-SY5Y cells

Popis výsledku v původním jazyce

Cadmium crosses the blood-brain barrier inducing damage to neurons. Cell impairment is predominantly linked to oxidative stress and glutathione (GSH) depletion. On the other hand, several reports have described an increase of GSH levels in neuronal cells after CdCl2 exposure. Therefore, the aim of the present report was to investigate the relation between changes in GSH levels and mitochondrial damage in neuronal cells after CdCl2 treatment. To characterize neuronal impairment after CdCl2 treatment (0-200 mu M) for 1-48 h, we used the SH-SY5Y cell line. We analyzed GSH metabolism and determined mitochondrial activity using high-resolution respirometry. CdCl2 treatment induced both the decreases and increases of GSH levels in SH-SY5Y cells. GSH concentration was significantly increased in cells incubated with up to 50 mu M CdCl2 but only 100 mu M CdCl2 induced GSH depletion linked to increased ROS production. The overexpression of proteins involved in GSH synthesis increased in response to 50 and 100 mu M CdCl2 after 6 h. Finally, strong mitochondrial impairment was detected even in 50 mu M CdCl2 treated cells after 24 h. We conclude that a significant decrease in mitochondrial activity can be observed in 50 mu M CdCl2 even without the occurrence of GSH depletion in SH-SY5Y cells.

Název v anglickém jazyce

Mitochondrial damage precedes the changes of glutathione metabolism in CdCl2 treated neuronal SH-SY5Y cells

Popis výsledku anglicky

Cadmium crosses the blood-brain barrier inducing damage to neurons. Cell impairment is predominantly linked to oxidative stress and glutathione (GSH) depletion. On the other hand, several reports have described an increase of GSH levels in neuronal cells after CdCl2 exposure. Therefore, the aim of the present report was to investigate the relation between changes in GSH levels and mitochondrial damage in neuronal cells after CdCl2 treatment. To characterize neuronal impairment after CdCl2 treatment (0-200 mu M) for 1-48 h, we used the SH-SY5Y cell line. We analyzed GSH metabolism and determined mitochondrial activity using high-resolution respirometry. CdCl2 treatment induced both the decreases and increases of GSH levels in SH-SY5Y cells. GSH concentration was significantly increased in cells incubated with up to 50 mu M CdCl2 but only 100 mu M CdCl2 induced GSH depletion linked to increased ROS production. The overexpression of proteins involved in GSH synthesis increased in response to 50 and 100 mu M CdCl2 after 6 h. Finally, strong mitochondrial impairment was detected even in 50 mu M CdCl2 treated cells after 24 h. We conclude that a significant decrease in mitochondrial activity can be observed in 50 mu M CdCl2 even without the occurrence of GSH depletion in SH-SY5Y cells.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

21101 - Food and beverages

Projekt

<a href="/cs/project/EF18_069%2F0010054" target="_blank" >EF18_069/0010054: IT4Neuro(degeneration)</a><br>

Návaznosti

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

Rok uplatnění

2024

Kód důvěrnosti údajů

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

Název periodika

Food and Chemical Toxicology

ISSN

0278-6915

e-ISSN

1873-6351

Svazek periodika

193

Číslo periodika v rámci svazku

November 2024

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

8

Strana od-do

114953

Kód UT WoS článku

001316970200001

EID výsledku v databázi Scopus

2-s2.0-85202788137