engleski

Dual Effects of Quercetin in Physiological Conditions and During Oxidative Injury in P19 Neurons

Oxidative stress is one of the major causes of neuronal death in a variety of neurodegenerative diseases. Dietary supplementation with quercetin, one of the most potent scavengers of reactive oxygen species (ROS), has been suggested as a potential therapeutic approach in both prevention and therapy of neuronal oxidative damage. As a growing number of evidence suggests that effects of antioxidants are not exclusively beneficial, we compared effects of high doses of quercetin in physiological conditions, and during oxidative injury induced by exposure of differentiated P19 neurons to hydrogen peroxide (H202). In physiological conditions quercetin reduced the elaborated network of neuritic processes, decreased basal level of ROS, depleted glutathione content, and induced changes in the expression of antiapoptotic gene Bcl-2. On the other hand, treatment with quercetin improved viability and morphological appearance of P19 neurons exposed to oxidative injury, and prevented H202-induced increase in ROS production, nuclear condensation and caspase-3/7 activation. The obtained results suggest beneficial effects of quercetin in neurons where oxidative stress-related neurodegenerative changes are already present, while quercetin-enriched supplements should be taken with caution in the prevention of oxidative injury. Accordingly, detailed pharmacological and toxicological studies, particularly in vivo, are required for quercetin-containing supplements in order to determine concentrations and time-window of administration that will be without side effects, but efficient in neuroprotection.

Morphological changes, hydrogen peroxide, reactive oxygen species, glutathione, caspase 3/7-activity, nuclear condensation, Bcl-2 expression

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