Antioxidants Targeting Mitochondrial Oxidative Stress: Promising Neuroprotectants for Epilepsy

Author:

Yang Nan1234,Guan Qi-Wen1234,Chen Fang-Hui5,Xia Qin-Xuan1234,Yin Xi-Xi6,Zhou Hong-Hao1234,Mao Xiao-Yuan1234ORCID

Affiliation:

1. Department of Clinical Pharmacology, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha 410008, China

2. Institute of Clinical Pharmacology, Central South University, Hunan Key Laboratory of Pharmacogenetics, 110 Xiangya Road, Changsha 410078, China

3. Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, 110 Xiangya Road, Changsha 410078, China

4. National Clinical Research Center for Geriatric Disorders, 87 Xiangya Road, Changsha, 410008 Hunan, China

5. Department of Pharmacy, The First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000 Jiangxi, China

6. Department of Pediatrics, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, 410008 Hunan, China

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.

Funder

Hunan Provincial Department of Education Innovation Platform Open Fund Project

Publisher

Hindawi Limited

Subject

Cell Biology,Ageing,General Medicine,Biochemistry

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