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线粒体中辅酶Q生化功能的更新

An updating of the biochemical function of coenzyme Q in mitochondria.

作者信息

Lenaz G, Fato R, Castelluccio C, Cavazzoni M, Estornell E, Huertas J F, Pallotti F, Parenti Castelli G, Rauchova H

机构信息

Dipartimento di Biochimica Giovanni Moruzzi, Universita' di Bologna, Italy.

出版信息

Mol Aspects Med. 1994;15 Suppl:s29-36. doi: 10.1016/0098-2997(94)90010-8.

DOI:10.1016/0098-2997(94)90010-8
PMID:7752842
Abstract

The apparent Km for coenzyme Q10 in NADH oxidation by coenzyme Q (CoQ)-extracted beef heart mitochondria is close to their CoQ content, whereas both succinate and glycerol-3-phosphate oxidation (the latter measured in hamster brown adipose tissue mitochondria) are almost saturated at physiological CoQ concentration. Attempts to enhance NADH oxidation rate by excess CoQ incorporation in vitro were only partially successful: the reason is in the limited amount of CoQ10 that can be incorporated in monomeric form, as shown by lack of fluorescence quenching of membrane fluorescent probes; at difference with CoQ10, CoQ5 quenches probe fluorescence and likewise enhances NADH oxidation rate above normal. Attempts to enhance the CoQ content in perfused rat liver and in isolated hepatocytes failed to show uptake in the purified mitochondrial fraction. Nevertheless CoQ cellular uptake is able to protect mitochondrial activities. Incubation of hepatocytes with adriamycin induces loss of respiration and mitochondrial potential measured in whole cells by flow cytometry using rhodamine 123 as a probe: concomitant incubation with CoQ10 completely protects both respiration and potential. An experimental study of aging in the rat has shown some decrease of mitochondrial CoQ content in heart, and less in liver and skeletal muscle. In spite of the little change observed, it is reasoned that CoQ administration may be beneficial in the elderly, owing to the increased demand for antioxidants.

摘要

辅酶Q(CoQ)提取的牛心线粒体中,辅酶Q10在NADH氧化反应中的表观米氏常数(Km)接近其CoQ含量,而琥珀酸和3-磷酸甘油氧化反应(后者在仓鼠棕色脂肪组织线粒体中测定)在生理CoQ浓度下几乎达到饱和。体外通过过量掺入CoQ来提高NADH氧化速率的尝试仅取得部分成功:原因在于以单体形式掺入的CoQ10数量有限,这可通过膜荧光探针缺乏荧光猝灭来证明;与CoQ10不同,CoQ5能猝灭探针荧光,同样也能将NADH氧化速率提高至正常水平以上。在灌注大鼠肝脏和分离的肝细胞中提高CoQ含量的尝试未能在纯化的线粒体组分中显示出摄取情况。然而,CoQ的细胞摄取能够保护线粒体活性。用阿霉素孵育肝细胞会导致呼吸作用丧失以及使用罗丹明123作为探针通过流式细胞术在全细胞中测量的线粒体电位降低:同时用CoQ10孵育可完全保护呼吸作用和电位。一项对大鼠衰老的实验研究表明,心脏中线粒体CoQ含量有所下降,肝脏和骨骼肌中下降较少。尽管观察到的变化很小,但由于对抗氧化剂的需求增加,推测补充CoQ可能对老年人有益。

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An updating of the biochemical function of coenzyme Q in mitochondria.线粒体中辅酶Q生化功能的更新
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