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Methotrexate (MTX) is commonly used as a chemotherapeutic drug against cancer but its efficacy is limited due to its side effects. Baicalin is a flavonoid that has potent antioxidant properties. This study aimed to evaluate baicalin’s protective effect on MTX-induced mitochondrial damage in testicular tissues of rats. Twenty-four male Wistar rats were distributed into four groups: control, MTX, MTX + baicalin, and baicalin alone. The activities of enzymes such as catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase was significantly lowered in the MTX treated group, compared to the other groups. Concomitantly, MTX group also showed elevated the levels of reactive oxygen species and thiobarbituric acid reactive substances in the testicular mitochondria. Furthermore, MTX group also showed reduced the activities of tricarboxylic acid (TCA) cycle enzymes, i.e., succinate dehydrogenase, malate dehydrogenase, isocitrate dehydrogenase, and alpha-ketoglutarate dehydrogenase. The actions of electron transport chain (ETC) complexes (I-IV), as well as mitochondrial membrane potential (MMP), were also reduced the MTX group. However, baicalin treatment reversed the damaging effect of MTX in the mitochondria of testicular tissues. The baicalin treatment potentially reduced the damaging impact of MTX in isolated mitochondria from testicular tissues. Thus, the current study revealed that the baicalin has conspicuous potential to attenuate the MTX induced mitochondrial damage in rat’s testicular tissues.

This research aimed to evaluate the curative impact of nobiletin (NOB) on paraquat (PQ) induced mitochondrial impairment in rats' hepatic tissues. Twenty-four male rats were divided into control, PQ, PQ + NOB, and NOB treated groups. The alanine aminotransferase levels, aspartate aminotransferase, and alkaline phosphatase were increased in the experimental animals after exposure with PQ. A significant decrease in the level of catalase, glutathione peroxidase, superoxide dismutase, glutathione, thiobarbituric acid reactive substances, and reactive oxygen species were recorded in rats exposed to PQ. The mitochondrial TCA cycle enzyme activities, including isocitrate-dehydrogenase, succinate-dehydrogenase, alpha-ketoglutarate dehydrogenase, and malate-dehydrogenase, were reduced in PQ exposed rats. The activities of mitochondrial enzymes including NADH dehydrogenase, coenzyme Q-cytochrome reductase, succinic-coenzyme Q and cytochrome c-oxidase were significantly decreased after the PQ-exposure. PQ administration also reduced the mitochondrial membrane potential. However, the administration of mitochondria with NOB can decrease the toxic effect of the PQ in isolated mitochondria. NOB treatment potentially reduced the damaging effects of the PQ in the mitochondria isolated from hepatic tissues. Thus, the current study revealed that the NOB could attenuate PQ-induced mitochondrial damage in rats' hepatic tissues.

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.