Key result
Quercetin pre-treatment significantly suppressed cisplatin-induced mitochondrial oxidative stress by decreasing lipid peroxidation and protein carbonyl levels (P<0.001) in isolated rat liver mitochondria.
Why the study?
Does quercetin prevent cisplatin-induced mitochondrial dysfunction in isolated rat liver mitochondria?
Does quercetin prevent cisplatin-induced mitochondrial dysfunction in isolated rat liver mitochondria?
p-value: p=<0.001
Quercetin supplementation may suppress cisplatin-induced mitochondrial toxicity, providing a potential prophylactic candidate against anticancer agent-induced oxidative stress.
Quercetin may attenuate cisplatin mitochondrial damage in vitro; hypothesis-generating and leaves clinical hepatoprotection open.
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 µg/ml CP and/or 50 µM 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.
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Waseem et al. (2017) studied Cisplatin-induced mitochondrial dysfunction (n=24). Quercetin vs. Cisplatin alone (100 µg/ml) was evaluated on Mitochondrial lipid peroxidation (LPO) and protein carbonyl (PC) levels (p=<0.001). Quercetin pre-treatment significantly suppressed cisplatin-induced mitochondrial oxidative stress by decreasing lipid peroxidation and protein carbonyl levels (P<0.001) in isolated rat liver mitochondria.
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