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2016 ; 12
(6
): 688-700
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Ubisol-Q10 Prevents Glutamate-Induced Cell Death by Blocking Mitochondrial
Fragmentation and Permeability Transition Pore Opening
#MMPMID27194946
Kumari S
; Mehta SL
; Milledge GZ
; Huang X
; Li H
; Li PA
Int J Biol Sci
2016[]; 12
(6
): 688-700
PMID27194946
show ga
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.