The involvement of calcium in the toxic effect of 4-methylethcathinone on SH-SY5Y cells

© 2023 John Wiley & Sons Ltd..

Neurotoxicity induced by psychoactive substances is often accompanied by an imbalance of intracellular calcium ions. It is unclear whether calcium ions play a role in the toxicity induced by psychoactive substances. In the present study, we aimed to evaluate the occurrence of calcium dysregulation and its contribution to cytotoxicity in human neurotypic SH-SY5Y cells challenged with a recently developed psychoactive substance 4-methylethcathinone (4-MEC). An increase in the intracellular calcium was detected by inductively coupled plasma atomic emission spectrometry and Fluo-3 AM dye in SH-SY5Y cells after being treated with 4-MEC. The increase of intracellular Ca2+ level mediated G0/G1 cell cycle arrest and ROS/endoplasmic reticulum stress-autophagy signaling pathways to achieve the toxicity of 4-MEC. In particular, N-acetyl-L-cysteine, a classical antioxidant, was found to be a potential treatment for 4-MEC-induced toxicity. Taken together, our results demonstrate that an increase in intracellular calcium content is one of the mechanisms of 4-MEC-induced toxicity. This study provides a molecular basis for the toxicity mechanism and therapeutic intervention of psychoactive substances.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:44

Enthalten in:

Journal of applied toxicology : JAT - 44(2024), 4 vom: 10. März, Seite 553-563

Sprache:

Englisch

Beteiligte Personen:

Zhang, Wei [VerfasserIn]
Cao, Fangqi [VerfasserIn]
Li, Ming [VerfasserIn]
Xu, Zhiwen [VerfasserIn]
Sun, Jing [VerfasserIn]
Huang, Zhiwei [VerfasserIn]
Shi, Ping [VerfasserIn]

Links:

Volltext

Themen:

4-methylethcathinone
9665W17SH3
Amphetamines
Autophagy
Calcium
Calcium ion
Endoplasmic reticulum stress
G0/G1 cell cycle arrest
Ions
Journal Article
Propiophenones
SY7Q814VUP

Anmerkungen:

Date Completed 19.03.2024

Date Revised 19.03.2024

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1002/jat.4560

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM364421622