International Journal Of Bilogical Sciences
.: Home > International Journal Of Bilogical Sciences > 2016 > Volume 12 Number 6 > Santosh Kumari1,4 *, Suresh L Mehta1,3*, Gaolin Z. Milledge2, Xinyu Huang2, Haining Li5, P. Andy Li1
Ubisol-Q10 Prevents Glutamate-Induced Cell Death by Blocking Mitochondrial Fragmentation and Permeability Transition Pore Opening
Santosh Kumari1,4 *, Suresh L Mehta1,3*, Gaolin Z. Milledge2, Xinyu Huang2, Haining Li5, P. Andy Li1
1. Department of Pharmaceutical Sciences, Biomanufacturing Research Institute and Technology Enterprise (BRITE) College of Art and Science, North Carolina Central University, Durham, NC 27707, USA; 2. Department of Mathematics and Computer Science, North Carolina Central University, Durham, NC 27707, USA; 3. Department of Neurological Surgery, University of Wisconsin, School of Medicine and Public Health, Madison, WI 53792, USA; 4. Department of Medicine, University of Wisconsin, School of Medicine and Public Health, Madison, WI 53792, USA. 5. Neurological Center of the General Hospital of Ningxia Medical University, Ningxia Key Laboratory for Cerebrocranial Diseases, Ningxia Medical University, Yinchuan, 750004, P.R. China. *Equal contribution Corresponding author: P. Andy Li, Department of Pharmaceutical Sciences , North Carolina Central University, BRITE Building 2025, 302 East Lawson Street, Durham, NC 27707. Fax: 919-530-6600 E-mail: firstname.lastname@example.org.
Mitochondrial dysfunction and oxidative stress are the major events that lead to the formation of mitochondrial permeability transition pore (mPTP) during glutamate-induced cytotoxicity and cell death. Coenzyme Q10 (CoQ10) has widely been used for the treatment of mitochondrial disorders and neurodegenerative diseases. Comparing to traditional lipid-soluble CoQ10, water soluble CoQ10 (Ubisol-Q10) has high intracellular and intra-mitochondrial distribution. The aims of the present study are to determine the neuroprotective effects of Ubisol-Q10 on glutamate-induced cell death and to explore its functional mechanisms. HT22 neuronal cells were exposed to glutamate. Cell viability was measured and mitochondrial fragmentation was assessed by mitochondrial imaging. The mPTP opening was determined by mitochondrial membrane potential and calcium retention capacity. The results revealed that the anti-glutamate toxicity effects of Ubisol-Q10 was associated with its ability to block mitochondrial fragmentation, to maintain calcium retention capacity and mitochondrial membrane potential, and to prevent mPTP formation, AIF release, and DNA fragmentation. We concluded that Ubisol-Q10 protects cells from glutamate toxicity by preserving the integrity of mitochondrial structure and function. Therefore, adequate CoQ10 supplementation may be beneficial in preventing cerebral stroke and other disorders that involve mitochondrial dysfunction.
Coenzyme Q10, glutamate toxicity, neuronal cell death, AIF, mitochondrial fragmentation, calcium retention.
Date Deposited : 04 Nov 2016 22:10
Official URL: http://www.ijbs.com/v12i6
Last Modified : 04 Nov 2016 22:10
Volume 12, Number 6, April 2016
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