TY - JOUR
AR - NNB-2019-1-101
TI - Effects of lithium treatment on oxidative stress markers in mitochondrial complex I and complex III inhibition and after CO2 exposure in SH-SY5Y cells
AU - Frederic M?rmol , Carrera 
AU - J, Sanchez
AU - Y. , Ferrero
JO - Neurology and Neurobiology
PY - 2019
DA - Thu 28, Feb 2019
SN - 2613-7828
DO - http://dx.doi.org/10.31487/j.NNB.2019.01.001
UR - https://www.sciencerepository.org/effects-of-lithium-treatment-on-oxidative-stress-markers-in-mitochondrial-complex-1-and-complex-3-inhibition-and-after-co2-exposure-in-sh-sy5y-cells_SR-NNB-2019-1-101 
KW - Lithium, SH-SY5Y, COX-2, Oxidative stress, Rotenone, CO2, Antimycin A
AB - 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