Specificity of coenzyme Q10 for a balanced function of respiratory chain and endogenous ubiquinone biosynthesis in human cells

被引:36
作者
Fernández-Ayala, DJM [1 ]
López-Lluch, G [1 ]
García-Valdés, M [1 ]
Arroyo, A [1 ]
Navas, P [1 ]
机构
[1] Univ Pablo de Olavide, CABD, Seville 43013, Spain
来源
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS | 2005年 / 1706卷 / 1-2期
关键词
coenzyme Q; mitochondria; ROS; respiratory chain; CoQ uptake;
D O I
10.1016/j.bbabio.2004.10.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Coenzyme Q (Q) is an obligatory component of both respiratory chain and uncoupling proteins. Also, Q acts as an antioxidant in cellular membranes. Several neurodegenerative diseases are associated with modifications of Q(10) levels. For these reasons, therapies based on Q supplementation in the diet are currently studied in order to mitigate the symptoms of these diseases. However, the incorporation of exogenous Q also affects aging process in nematodes probably affecting reactive oxygen species (ROS) production. The aim of the present work is to clarify if supplementation with both Q(10) and Q(6) isoforms affects mitochondrial Q(10) content, respiratory chain activity and ROS levels in human cells. Cells incorporated exogenously added Q(10) and Q(6) isoforms into mitochondria that produced changes in mitochondrial activity depending on the side chain length. Supplementation with Q(10), but not with Q(6), increased mitochondrial Q-dependent activities. However, Q(6) affected the mitochondrial membrane potential, ROS production, and increased the protein levels of both catalase and Mn-superoxide dismutase (Mn-SOD). Also, Q(6) induced a transient decrease in endogenous mitochondrial Q(10) levels by increasing its catabolism. These results show that human cells supplemented with Q(6) undergo a mitochondrial impairment, which is not observed with Q(10) supplementation. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:174 / 183
页数:10
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