Abstract
Mitochondria are major sources of reactive oxygen species (ROS) within the cell and are especially vulnerable to oxidative stress. Oxidative damage to mitochondria results in disrupted mitochondrial function and cell death signaling, finally triggering diverse pathologies such as epilepsy, a common neurological disease characterized with aberrant electrical brain activity. Antioxidants are considered as promising neuroprotective strategies for epileptic condition via combating the deleterious effects of excessive ROS production in mitochondria. In this review, we provide a brief discussion of the role of mitochondrial oxidative stress in the pathophysiology of epilepsy and evidences that support neuroprotective roles of antioxidants targeting mitochondrial oxidative stress including mitochondria-targeted antioxidants, polyphenols, vitamins, thiols, and nuclear factor E2-related factor 2 (Nrf2) activators in epilepsy. We point out these antioxidative compounds as effectively protective approaches for improving prognosis. In addition, we specially propose that these antioxidants exert neuroprotection against epileptic impairment possibly by modulating cell death interactions, notably autophagy-apoptosis, and autophagy-ferroptosis crosstalk.
Highlights
Mitochondria are major sources of reactive oxygen species (ROS) within the cell and are especially vulnerable to oxidative stress
We provide a brief discussion of the role of mitochondrial oxidative stress in the pathophysiology of epilepsy and evidences that support neuroprotective roles of antioxidants targeting mitochondrial oxidative stress including mitochondria-targeted antioxidants, polyphenols, vitamins, thiols, and nuclear factor E2-related factor 2 (Nrf2) activators in epilepsy
The evidence discussed in the review supports that mitochondrial oxidative stress and dysfunction are implicated in the onset and progress of epilepsy
Summary
There are a plethora of investigations supporting that mitochondrial dysfunction forms an integral part of the development of neurological disorders and in particular epilepsy, a debilitating disease characterized by recurrent unprovoked seizures [1,2,3,4]. Enhanced activities of enzymes such as glutathione peroxidase (GPx) and glutathione reductase (GR) in mitochondria have been demonstrated to exert neuroprotective effects against ROS-triggered oxidative damage in patients with epilepsy [8]. These data indicate that oxidative mitochondria damage can be diminished with clinical benefits by augmenting the activity of mitochondrial antioxidant enzymes. Antioxidants have the ability to counteract the deleterious effects of ROS and exert great benefits on oxidative stress-associated malformations including epilepsy. We propose that modulation of interplay of distinct cell death modes is likely to be a critical mechanism for mitochondrially targeted antioxidants
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
