Quinolinic Acid Impairs Redox Homeostasis, Bioenergetic, and Cell Signaling in Rat Striatum Slices: Prevention by Coenzyme Q 10

Quinolinic acid (QUIN) is an important agonist of NMDA receptors that are found at high levels in cases of brain injury and neuroinflammation. Therefore, it is necessary to investigate neuroprotection strategies capable of neutralizing the effects of the QUIN on the brain. Coenzyme Q (CoQ ) is a pro...

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Bibliographic Details
Published in:Neurotoxicity research 2022-04, Vol.40 (2), p.473
Main Authors: Ferreira, Fernanda Silva, Dos Santos, Tiago Marcon, Ramires Junior, Osmar Vieira, Silveira, Josiane Silva, Schmitz, Felipe, Wyse, Angela T S
Format: Article
Language:English
Subjects:
Acetylcholinesterase - metabolism
Animals
Antioxidants - metabolism
Antioxidants - pharmacology
Energy Metabolism
Homeostasis
Oxidation-Reduction
Quinolinic Acid - toxicity
Rats
Rats, Wistar
Signal Transduction
Ubiquinone - pharmacology
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Summary:Quinolinic acid (QUIN) is an important agonist of NMDA receptors that are found at high levels in cases of brain injury and neuroinflammation. Therefore, it is necessary to investigate neuroprotection strategies capable of neutralizing the effects of the QUIN on the brain. Coenzyme Q (CoQ ) is a provitamin that has an important antioxidant and anti-inflammatory action. This work aims to evaluate the possible neuroprotective effect of CoQ against the toxicity caused by QUIN. Striatal slices from 30-day-old Wistar rats were preincubated with CoQ 25-100 μM for 15 min; then, QUIN 100 μM was added to the incubation medium for 30 min. A dose-response curve was used to select the CoQ concentration to be used in the study. Results showed that QUIN caused changes in the production of ROS, nitrite levels, activities of antioxidant enzymes, glutathione content, and damage to proteins and lipids. CoQ was able to prevent the effects caused by QUIN, totally or partially, except for damage to proteins. QUIN also altered the activities of electron transport chain complexes and ATP levels, and CoQ prevented totally and partially these effects, respectively. CoQ prevented the increase in acetylcholinesterase activity, but not the decrease in the activity of Na ,K -ATPase caused by QUIN. We also observed that QUIN caused changes in the total ERK and phospho-Akt content, and these effects were partially prevented by CoQ . These findings suggest that CoQ may be a promising therapeutic alternative for neuroprotection against QUIN neurotoxicity.
ISSN:1476-3524