Effects of lithium treatment on oxidative stress markers in mitochondrial complex I and complex III inhibition and after CO2 exposure in SH-SY5Y cells

Effects of lithium treatment on oxidative stress markers in mitochondrial complex I and complex III inhibition and after CO2 exposure in SH-SY5Y cells

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Author Info

Corresponding Author
Frederic M?rmol Carrera
Unitat de Farmacologia, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain

A B S T R A C T

This study aims to evaluate the effects of lithium chloride (LiCl) on resistance to oxidative stress, cell proliferation, and COX-2 expression, both in the absence of carbon dioxide (CO2), rotenone and antimycin A and after exposure to them. SH-SY5Y cells were treated for 72 hours with LiCl (0.5 - 5 mM). Superoxide anion (O2 - ) and intracellular reactive oxygen species (ROS) production were measured via fluorescence. All the experiments were carried out under standard conditions, after 4 h of CO2 exposure or after 24 hours of incubation with rotenone and antimycin A: inhibitors of mitochondrial complex I and III respectively. At very low concentrations, LiCl decreased O2 - production under normoxic conditions and after exposure to either CO2 or rotenone. LiCl was not observed to produce any changes in intracellular ROS levels under standard conditions or after either the rotenone or antimycin A treatment; but changes were observed after CO2 exposure. In addition, LiCl increased cell proliferation and modified expression of COX-2, but only under oxidative stress situations. In conclusion, the antioxidant effect of lithium might be due, at least in part, to its inhibition of O2 - from complex I. Also, lithium decreases the vulnerability of SH-SY5Y cells to cell injury

Article Info

Article Type
Research Article
Publication history
Received: Fri 25, Jan 2019
Accepted: Wed 13, Feb 2019
Published: Thu 28, Feb 2019
Copyright
© 2023 Frederic M?rmol Carrera . This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Hosting by Science Repository.
DOI: 10.31487/j.NNB.2019.01.001