Chemotherapy induces an increase in coenzyme Q10 levels in cancer cell lines

被引：49

作者：

Brea-Calvo, G ^{[1
]}

Rodríguez-Hernández, A ^{[1
]}

Fernández-Ayala, DJM ^{[1
]}

Navas, P ^{[1
]}

Sánchez-Alcázar, JA ^{[1
]}

机构：

[1] Univ Pablo Olavide, Ctr Andaluz Biol Desarrollo, Seville 41013, Spain

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 2006年 / 40卷 / 08期

关键词：

coenzyme Q; apoptosis; chemotherapy; reactive oxygen species; free radical;

D O I：

10.1016/j.freeradbiomed.2005.11.014

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：

Free radicals have been implicated in the action of many chemotherapeutic drugs. Here we tested the hypothesis that camptothecin and other chemotherapeutic drugs, such as etoposide, doxorubicin, and methotrexate, induce an increase in coenzyme Q(10) levels as part of the antioxidant defense against tree radical production under these anticancer treatments in cancer cell lines. Chemotherapy treatment induced both free radical production and an increase in coenzyme Q(10) levels in all the cancer cell lines tested. Reduced coenzyme Q(10) form levels were particularly enhanced. Coenzyme Q(10)-increased levels were associated with tip-regulation of COQ genes expression, involved in coenzyme Q(10) biosynthesis. At the translational level, COQ7 protein expression levels were also increased. Furthermore, coenzyme Q(10) biosynthesis inhibition blocked camptothecin-induced coenzyme Q(10) increase, and enhanced camptothecin cytotoxicity. Our findings suggest that coenzyme Q(10) increase is implicated in the cellular defense under chemotherapy treatment and may contribute to cell survival. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：1293 / 1302

页数：10

共 56 条

[1] Mechanism of lovastatin-induced apoptosis in intestinal epithelial cells [J].

Agarwal, B ;

Halmos, B ;

Feoktistov, AS ;

Protiva, P ;

Ramey, WG ;

Chen, M ;

Pothoulakis, C ;

Lamont, JT ;

Holt, PR .

CARCINOGENESIS, 2002, 23 (03) :521-528

[2]

Agarwal B, 1999, CLIN CANCER RES, V5, P2223

[3] 4-HYDROXYBENZOATE - POLYPRENYL TRANSFERASE AND PRENYLATION OF 4-AMINOBENZOATE IN MAMMALIAN-TISSUES [J].

ALAM, SS ;

NAMBUDIRI, AMD ;

RUDNEY, H .

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1975, 171 (01) :183-190

[4]

ALBINA JE, 1993, J IMMUNOL, V150, P5080

[5] Coenzyme Q blocks biochemical but not receptor-mediated apoptosis by increasing mitochondrial antioxidant protection [J].

Alleva, R ;

Tomasetti, M ;

Andera, L ;

Gellert, N ;

Borghi, B ;

Weber, C ;

Murphy, MP ;

Neuzil, J .

FEBS LETTERS, 2001, 503 (01) :46-50

[6] Silencing of ubiquinone biosynthesis genes extends life span in Caenorhabditis elegans [J].

Asencio, C ;

Rodríguez-Aguilera, JC ;

Ruiz-Ferrer, M ;

Vela, J ;

Navas, P .

FASEB JOURNAL, 2003, 17 (06) :1135-+

[7] Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization [J].

Bossy-Wetzel, E ;

Newmeyer, DD ;

Green, DR .

EMBO JOURNAL, 1998, 17 (01) :37-49

[8]

Bouterfa HL, 2000, ANTICANCER RES, V20, P2761

[9] OXIDATIVE STRESS AS A MEDIATOR OF APOPTOSIS [J].

BUTTKE, TM ;

SANDSTROM, PA .

IMMUNOLOGY TODAY, 1994, 15 (01) :7-10

[10]

Chan KKW, 2003, CLIN CANCER RES, V9, P10

← 1 2 3 4 5 6 →