Abstract
Oxidative stress has been implicated as one of the causes in cell death in many neurodegenerative disorders. Due to antioxidative properties in vitro, the use of flavonoids and other polyphenolic compounds synthesised by plants are considered to be a promising strategy to prevent Alzheimer’s disease and Parkinsons’s disease. In the present study, we tested protective effects of some polyphenols and sodium pyruvate on 6-hydroxydopamine (6-OHDA), salsolinol and 3-hydroxykynurenine (3-HK) induced neurotoxicity in human neuroblastoma SH-SY5Y cells. We found that luteolin prevented from 6-OHDA and 3-HK induced cell viability reduction and that one of the mechanisms involved in the neuroprotective process was the ability to increase the level of cellular ATP. However, luteolin was ineffective against salsolinol-induced toxicity. Neither pre-treatment with flavonoids nor simultaneous addition had any protective effects on 6-OHDA, salsolinol or 3-HK induced neurotoxicity. Interestingly, both pre-treatment and co-treatment with pyruvate provided protection against 6-OHDA, salsolinol or 3-HK induced toxicity. Moreover, luteolin and sodium pyruvate, administered together, acted additively, so to achieve the same effect, lower concentrations were needed. The ability of luteolin and sodium pyruvate to reduce toxicity of 6-OHDA and 3-HK in SH-SY5Y cells may be related to two different neuroprotective mechanisms and the capability to penetrate into the cell.
Highlights
Oxidative stress is induced by an imbalance between the production of reactive oxygen species (ROS) and the detoxification of reactive intermediates in mitochondria and has been strongly implicated as one of the causes and triggering factors of cell death
An effective toxic dose of 6-OHDA after 24 hours treatment was observed at about 75 μM in MTT assay and 50 μM in ATP and CellTiter-Glo cell viability assay resulted in about 50% cell death
In the present study we intended to evaluate structurally diverse plant phenolics for their abilities to reduce neurotoxicity induced by substances with different mode of action in SH-SY5Y human neuroblastoma cell line
Summary
Oxidative stress is induced by an imbalance between the production of reactive oxygen species (ROS) and the detoxification of reactive intermediates in mitochondria and has been strongly implicated as one of the causes and triggering factors of cell death. ROS are highly reactive and toxic reduced oxygen forms such as hydrogen peroxide (H2O2), superoxide radical ( O2 ) and hydroxyl radical (OH–) continuously generate in the mitochondrial respiratory chain, in which energy is produced in the form of adenosine-5’-triphosphate (ATP). The only available defence against ROS in mitochondria are enzymes (for example superoxide dismutase, catalase, peroxidase) or low molecular weight oxidants (e.g. chelating agents, glutathione, NADPH). Generated oxidative stress may be reduced through agents from dietary sources. Since flavonoids, polyhydroxylated phytochemicals and common dietary components present in fruits, vegetables and beverages like tea or wine, have
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