Protection by Exogenously Added Coenzyme Q(9) against Free Radical-Induced Injuries in Human Liver Cells.
Protection by Exogenously Added Coenzyme Q(9) against Free Radical-Induced Injuries in Human Liver Cells.
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DOI：
10.3164/jcbn.09-128
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发表时间：
2010-05
影响因子：
2.4
通讯作者：
Matsura T
中科院分区：
文献类型：
--
作者：
Kusumoto C;Kinugawa T;Morikawa H;Teraoka M;Nishida T;Murawaki Y;Yamada K;Matsura T
还原辅酶Q10 （CoQ10H2）在生物系统中被认为是一种有效的抗氧化剂。然而，目前尚不清楚辅酶q9h2是否能在人体细胞中作为抗氧化剂。本研究的目的是评估外源性添加辅酶q9是否可以保护人肝细胞免受水溶性自由基引发剂2,2'-偶氮（2-脒基丙烷）二盐酸（AAPH）和脂溶性自由基引发剂2,2'-偶氮（2,4-二甲基戊腈）（AMVN）的损伤。用10µM CoQ9脂质体处理HepG2细胞24 h，获得CoQ9富集细胞。将CoQ9富集细胞分别暴露于10 mM AAPH和500µM AMVN中4 h和24 h。coq9富集的细胞在AAPH或AMVN处理后的活力丧失比未处理的HepG2细胞少得多。在coq9富集的细胞中，AAPH或AMVN处理后谷胱甘肽的减少和硫代巴比妥酸反应物质的增加也受到抑制。与AAPH或AMVN孵育CoQ9富集的细胞，导致细胞中CoQ9H2的减少和细胞中CoQ9的相互增加，这是由于其抗氧化功能。综上所述，这是首次证明外源性添加CoQ9可以通过其抗氧化活性来防止氧化应激介导的人体细胞损伤。
Reduced coenzyme Q10 (CoQ10H2) is known as a potent antioxidant in biological systems. However, it is not yet known whether CoQ9H2 could act as an antioxidant in human cells. The aim of this study is to assess whether exogenously added CoQ9 can protect human liver cells against injuries induced by a water-soluble radical initiator, 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) and a lipid-soluble radical initiator, 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN). CoQ9-enriched cells were obtained by treatment of HepG2 cells with 10 µM CoQ9 liposomes for 24 h. CoQ9-enriched cells were exposed to 10 mM AAPH and 500 µM AMVN over 4 h and 24 h, respectively. The loss of viability after treatment with AAPH or AMVN was much less in CoQ9-enriched cells than in naive HepG2 cells. The decrease in glutathione and the increase in thiobarbituric acid-reactive substance after treatment with AAPH or AMVN were also suppressed in CoQ9-enriched cells. The incubation of CoQ9-enriched cells with AAPH or AMVN led to a decrease in cellular CoQ9H2 and reciprocal increase in cellular CoQ9 resulting from its antioxidant function. Taken together, it was demonstrated for the first time that exogenously added CoQ9 could prevent oxidative stress-mediated damage to human cells by virtue of its antioxidant activity.
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DOI：
10.1016/0005-2760(92)90232-k
发表时间：
1992-08-19
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA
影响因子：
--
作者：
MATSURA, T;YAMADA, K;KAWASAKI, T
通讯作者：
KAWASAKI, T
影响因子：
4.4
作者：
Sohal, Rajindar S.;Forster, Michael J.
通讯作者：
Forster, Michael J.
影响因子：
2.4
作者：
Kettawan, Aikkarach;Takahashi, Takayuki;Okamoto, Tadashi
通讯作者：
Okamoto, Tadashi
影响因子：
3.5
作者：
Matsura, T;Serinkan, BF;Kagan, VE
通讯作者：
Kagan, VE
影响因子：
2.4
作者：
Schmelzer C;Lorenz G;Rimbach G;Döring F
通讯作者：
Döring F