Low level laser therapy reduces oxidative stress in cortical neurons in vitro
2012
It is accepted that the mechanisms of low level laser therapy (LLLT) involves photons that are absorbed in the
mitochondria of cells and lead to increase of mitochondrial metabolism resulting in more electron transport, increase
of mitochondrial membrane potential, and more ATP production. Intracellular calcium changes are seen that
correlate with mitochondrial stimulation. The situation with two other intermediates is more complex however:
reactive oxygen species (ROS) and nitric oxide (NO). Evidence exists that low levels of ROS are produced by LLLT
in normal cells that can be beneficial by (for instance) activating NF-kB. However high fluences of light can
produce large amounts of ROS that can damage the cells. In oxidatively stressed cells the situation may be different.
We exposed primary cultured cortical neurons to hydrogen peroxide (H 2 O 2 ) or cobalt chloride (CoCl 2 ) oxidative
insults in the presence or absence of LLLT (810-nm laser at 0.3 or 3 J/cm 2 ). Cell viability of cortical neurons was
determined by lactate dehydrogenase assay. ROS in neurons was detected using an ROS probe, MitoRox with
confocal microscopy. Results showed that LLLT dose-dependently reversed ROS production and protected cortical
neurons against H 2 O 2 or CoCl 2 induced oxidative injury in cultured cortical neurons. Conclusion: LLLT can protect
cortical neurons against oxidative stress by reversing the levels of ROS.
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