Ameliorative effects of morin on cisplatin-induced toxicity in renal mitochondria isolated from rats

Abstract

Cisplatin (CP) is the most effective chemotherapeutic drug used to treat various types of solid tumors. Morin is a natural flavonoid having a wide range of pharmacological properties. This investigation was aimed to explore the curative effect of morin against CP persuaded mitochondrial dysfunction in renal tissues of rats. Adult male Sprague-Dawley rats (n = 24) were randomly distributed into four groups for this experiment; control group, CP administered group, CP + morin administered group, and morin administered group. The results showed adverse effects of CP on renal biomarkers by elevating and reducing the level of urea, creatinine, and creatinine clearance sequentially. The antioxidant enzymatic and non-enzymatic activities, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione (GSH) levels were significantly decreased in renal mitochondria of CP-exposed rats. CP administration significantly elevated the ROS and TBARS levels. CP administration remarkably reduced TCA cycle enzymes activity, including succinate dehydrogenase (SDH), malate dehydrogenase (MDH), isocitrate dehydrogenase (ICDH) and alpha-ketoglutarate dehydrogenase (α-KGDH). Moreover, mitochondrial electron transport chain (ETC) enzymes, such as succinic-coenzyme Q, NADH dehydrogenase, Cytochrome c-oxidase, and coenzyme Q-cytochrome reductase activities, were also reduced after CP treatment. CP-induction significantly reduced the mitochondria membrane potential (ΔΨm). Nonetheless, morin supplementation significantly ameliorated the damaging impacts of CP in isolated mitochondria from renal tissues of rats. Thus, the present study revealed that the morin has conspicuous potential to attenuate the CP-instigated mitochondrial injuries in the renal tissues of adult male Sprague-Dawley rats.