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Clioquinol rescues yeast cells from Aβ42 toxicity via the inhibition of oxidative damage. | LitMetric

AI Article Synopsis

  • Researchers investigated the effects of clioquinol (CQ), a potential Alzheimer's treatment, on yeast cells expressing Aβ42, showing it can reduce Aβ42 toxicity.
  • CQ lowered reactive oxygen species (ROS) and lipid peroxidation by increasing levels of reduced glutathione (GSH), independently of certain antioxidant enzymes.
  • The study uncovered CQ's unique role in affecting antioxidant enzyme activity and restoring GSH balance, which may help in developing new drug treatments for Alzheimer's disease.

Article Abstract

Alzheimer's disease (AD), the most common form of dementia, has gotten considerable attention. Previous studies have demonstrated that clioquinol (CQ) as a metal chelator is a potential drug for the treatment of AD. However, the mode of action of CQ in AD is still unclear. In our study, the antioxidant effects of CQ on yeast cells expressing Aβ42 were investigated. We found that CQ could reduce Aβ42 toxicity by alleviating reactive oxygen species (ROS) generation and lipid peroxidation level in yeast cells. These alterations were mainly attributable to the increased reduced glutathione (GSH) content and independent of activities of superoxide dismutase (SOD) and/or catalase (CAT). CQ could affect antioxidant enzyme activity by altering the transcription level of related genes. Interestingly, it was noted for the first time that CQ could combine with antioxidant enzymes to reduce their enzymatic activities by molecular docking and circular dichroism spectroscopy. In addition, CQ restored Aβ42-mediated disruption of GSH homeostasis via regulating YAP1 expression to protect cells against oxidative stress. Our findings not only improve the current understanding of the mechanism of CQ as a potential drug for AD treatment but also provide ideas for subsequent drug research and development.

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Source
http://dx.doi.org/10.1002/biot.202300662DOI Listing

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