Effect of quercetin on daunorubicin-induced heart mitochondria changes in rats

被引:27
作者
Guzy, J
Kusnír, J
Mareková, M
Chavková, Z
Dubayová, K
Mojzisová, G
Mirossay, L
Mojzis, J [1 ]
机构
[1] Safarik Univ, Fac Med, Dept Pharmacol, Tr SNP 1, Kosice 04066, Slovakia
[2] Safarik Univ, Fac Med, Dept Med Chem & Biochem, Kosice 04066, Slovakia
[3] Safarik Univ, Fac Med, Dept Expt Med, Kosice 04066, Slovakia
关键词
mitochondria; antioxidant enzymes; daunorubicin; quercetin; synchronous fluorescence spectra;
D O I
10.33549/physiolres.930413
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Cancer therapy with daunorubicin is limited by its cardiotoxicity. It has been suggested that daunorubicin-induced free radical generation can be involved. The precise molecular mechanism of daunorubicin-induced cardiotoxicity is still not well understood but it is believed that mitochondria play an important role in this process. It has been reported that flavonoids with antioxidant properties may prevent anthracycline-induced cardiotoxicity. In this work, we investigated the effects of daunorubicin and quercetin on mitochondrial enzyme activities such as ATPase, glutathione peroxidase (GPx) and glutathione reductase (GR). Moreover, we also studied the changes of outer mitochondrial membrane using synchronous fluorescence spectra. The actitivity of ATPase and GR were significantly increased after daunorubicin application. Pretreatment with quercetin significantly alleviated this increase. On the other hand, GPx activity was significantly decreased and quercetin prevented this decrease. Treatment with quercetin alone had no significant effect on the enzyme activity studied. Quercetin also completely prevented daunorubicin-induced changes in fluorescence of the outer mitochondrial membrane. In conclusion, our data indicate that quercetin may be useful in mitigating daunorubicin-induced cardiotoxicity.
引用
收藏
页码:773 / 780
页数:8
相关论文
共 55 条
[1]   CHELATING AND FREE-RADICAL SCAVENGING MECHANISMS OF INHIBITORY-ACTION OF RUTIN AND QUERCETIN IN LIPID-PEROXIDATION [J].
AFANASEV, IB ;
DOROZHKO, AI ;
BRODSKII, AV ;
KOSTYUK, VA ;
POTAPOVITCH, AI .
BIOCHEMICAL PHARMACOLOGY, 1989, 38 (11) :1763-1769
[2]  
ALLEN A, 1992, SEMIN ONCOL, V19, P529
[3]  
[Anonymous], 2000, ENCY ANAL CHEM
[4]   Sarcoplasmic reticulum genes are selectively down-regulated in cardiomyopathy produced by doxorubicin in rabbits [J].
Arai, M ;
Tomaru, K ;
Takizawa, T ;
Sekiguchi, K ;
Yokoyama, T ;
Suzuki, T ;
Nagai, R .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1998, 30 (02) :243-254
[5]  
CARLBERG I, 1985, METHOD ENZYMOL, V113, P484
[6]   A DIGITIZED-FLUORESCENCE-IMAGING STUDY OF MITOCHONDRIAL CA2+ INCREASE BY DOXORUBICIN IN CARDIAC MYOCYTES [J].
CHACON, E ;
ULRICH, R ;
ACOSTA, D .
BIOCHEMICAL JOURNAL, 1992, 281 :871-878
[7]   On the ability of four flavonoids, baicilein, luteolin, naringenin, and quercetin, to suppress the fenton reaction of the iron-ATP complex [J].
Cheng, IF ;
Breen, K .
BIOMETALS, 2000, 13 (01) :77-83
[8]  
DAVIES KJA, 1986, J BIOL CHEM, V261, P3060
[9]  
DOROSHOW JH, 1983, CANCER RES, V43, P4543
[10]   ENZYMATIC DEFENSES OF THE MOUSE HEART AGAINST REACTIVE OXYGEN METABOLITES - ALTERATIONS PRODUCED BY DOXORUBICIN [J].
DOROSHOW, JH ;
LOCKER, GY ;
MYERS, CE .
JOURNAL OF CLINICAL INVESTIGATION, 1980, 65 (01) :128-135