Ubiquinone-1 is an intermediate in the biosynthetic pathway of coenzyme Q[1]. Ubiquinone-1 is mainly reduced to ubiquinol by the action of complex I and II in the mitochondrial respiratory chain, acting as an electron carrier in the inner mitochondrial membrane to mediate electron transfer within the aerobic respiratory chain, promote oxidative phosphorylation and generate ATP and energy for cells[2]. Ubiquinone-1 also plays a role in antioxidant defense by scavenging reactive oxygen species (ROS) and reducing oxidative stress damage[3]. Ubiquinone-1 is usually used in research on energy metabolism and neurological diseases, immune system diseases[4][5].
In vitro, treatment of rat pulmonary microvascular endothelial cells (PMVEC) cultured in low glucose medium with Ubiquinone-1 (10µM; 6h) prevented ATP depletion, mitochondrial membrane depolarization, and increased monolayer permeability caused by the complex I inhibitor rotenone[6]. Treatment of primary rat astrocyte cultures with Ubiquinone-1 (5µM; 30min) significantly inhibited the recycling of ascorbate from dehydroascorbic acid (DHAA) in a dose-dependent manner under glucose-free conditions[7].
References:
[1] Fato R, Estornell E, Di Bernardo S, Pallotti F, Parenti Castelli G, Lenaz G. Steady-state kinetics of the reduction of coenzyme Q analogs by complex I (NADH:ubiquinone oxidoreductase) in bovine heart mitochondria and submitochondrial particles. Biochemistry. 1996;35(8):2705-2716.
[2] Mantle D, Dewsbury M, Hargreaves IP. The Ubiquinone-Ubiquinol Redox Cycle and Its Clinical Consequences: An Overview. Int J Mol Sci. 2024;25(12):6765.
[3] Olaru G, Buga AM, Sandu RE, Padureanu V, Popa DG, Calina D. Harnessing Mitochondrial Function for Post-Stroke Rehabilitation: Unlocking Antioxidant Power. Antioxidants (Basel). 2025;14(9):1080.
[4] Roginsky VA, Mohr D, Stocker R. Reduction of ubiquinone-1 by ascorbic acid is a catalytic and reversible process controlled by the concentration of molecular oxygen. Redox Rep. 1996;2(1):55-62.
[5] Rauchova H. Coenzyme Q10 effects in neurological diseases. Physiol Res. 2021;70(Suppl4):S683-S714.
[6] Bongard RD, Townsley MI, Merker MP. The effects of mitochondrial complex I blockade on ATP and permeability in rat pulmonary microvascular endothelial cells in culture (PMVEC) are overcome by coenzyme Q1 (CoQ1). Free Radic Biol Med. 2015;79:69-77.
[7] Dragan M, Dixon SJ, Jaworski E, Chan TS, O'brien PJ, Wilson JX. Coenzyme Q(1) depletes NAD(P)H and impairs recycling of ascorbate in astrocytes. Brain Res. 2006;1078(1):9-18.
Ubiquinone-1是辅酶Q合成过程中的中间体[1]。Ubiquinone-1主要通过细胞呼吸链中的复合体I和II的作用被还原为Ubiquinol，在线粒体内膜中作为电子载体，介导有氧呼吸链内的电子传递，促进氧化磷酸化，生成ATP，为细胞提供能量[2]。Ubiquinone-1还通过清除活性氧（ROS）和减少氧化应激损伤在抗氧化防御中发挥作用[3]。Ubiquinone-1通常用于能量代谢以及神经系统疾病、免疫系统疾病的研究[4][5]。
在体外实验中，用Ubiquinone-1（10µM；6小时）处理低葡萄糖培养基中的大鼠肺微血管内皮细胞（PMVEC），可阻止由复合体I抑制剂鱼藤酮引起的ATP耗竭、线粒体膜电位去极化以及单层通透性增加[6]。在无葡萄糖条件下，用Ubiquinone-1（5µM；30分钟）处理原代大鼠星形胶质细胞培养物，以剂量依赖的方式显著抑制脱氢抗坏血酸（DHAA）到抗坏血酸的再循环[7]。