Ameliorative efficacy of quercetin against cisplatin-induced mitochondrial dysfunction: Study on isolated rat liver mitochondria

被引:15
|
作者
Waseem, Mohammad [1 ]
Tabassum, Heena [2 ]
Bhardwaj, Monica [1 ]
Parvez, Suhel [1 ]
机构
[1] Jamia Hamdard, Dept Med Elementol & Toxicol, New Delhi 110062, India
[2] Jamia Hamdard, Dept Biochem, New Delhi 110062, India
关键词
cisplatin; quercetin; mitochondria; antioxidants; mitochondrial stress; OXIDATIVE STRESS; INDUCED APOPTOSIS; CANCER CELLS; IN-VITRO; ANTIOXIDANT; HEPATOTOXICITY; DAMAGE; DNA; NEPHROTOXICITY; ENZYMES;
D O I
10.3892/mmr.2017.6860
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The present study aimed to investigate the hepatoprotective effects of the bioflavonoid quercetin (QR) on cisplatin (CP)-induced mitochondrial oxidative stress in the livers of rats, to elucidate the role of mitochondria in CP-induced hepatotoxicity, and its underlying mechanism. Isolated liver mitochondria were incubated with 100 mu g/ml CP and/or 50 mu M QR in vitro. CP treatment triggered a significant increase in membrane lipid peroxidation (LPO) levels, protein carbonyl (PC) contents, and a decrease in reduced glutathione (GSH) and non-protein thiol (NP-SH) levels. In addition, CP caused a marked decline in the activities of enzymatic antioxidants and mitochondrial complexes (I, II, III and V) in liver mitochondria. QR pre-treatment significantly modulated the activities of enzymatic antioxidants and mitochondrial complex enzymes. Furthermore, QR reversed the alterations in LPO and PC levels, and GSH and NP-SH contents in liver mitochondria. The results of the present study suggested that QR supplementation may suppress CP-induced mitochondrial toxicity during chemotherapy, and provides a potential prophylactic and defensive candidate for anticancer agent-induced oxidative stress.
引用
收藏
页码:2939 / 2945
页数:7
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