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Food Chem Toxicol. 2013 Aug;58:388-93. doi: 10.1016/j.fct.2013.05.005. Epub 2013 May 15.

Protective role of phosphatidylcholine against cisplatin-induced renal toxicity and oxidative stress in rats.

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Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul 156-756, Republic of Korea.


Although cisplatin is widely used in the treatment of cancers, clinical use of cisplatin is limited due to its nephrotoxicity. Pathophysiological mechanism of cisplatin-induced renal toxicity is a complex process and has not been fully understand. Reactive oxygen species (ROS) and oxidative stress have been presumed to be involved in this damage process. Phosphatidylcholine (PC) has antioxidant effect and prevents oxidative stress. Therefore, the present study aimed to investigate potential protective effects of PC on cisplatin-induced renal damage in rat. We examined the protective effects of PC on cisplatin-induced renal damage by assessment of serum creatinine, BUN, lipid peroxidation, total glutathione, glutathione peroxidase activity, catalase activity, superoxide dismutase activity and histophathological changes. PC ameliorated cisplatin-induced increases in serum creatinine, urea and oxidative stress. PC also decreased tubular degeneration and hypertrophy of glomeruli. PC may have a protective effect against cisplatin-induced nephrotoxicity in rats via enhancing antioxidant enzyme activity.


ARF; Acute renal failure; BUN; CAT; Cisplatin; GPx; GR; GSH; MDA; Oxidative stress; PAS; PC; PMN; Phosphatidylcholine; ROS; Renal toxicity; SOD; acute renal failure; blood urea nitrogen; catalase; glutathione; glutathione peroxidase; glutathione reductase; malondialdehyde; periodic acid-Schiff; phosphatidylcholine; polymorphonuclear leukocytes; reactive oxygen species; superoxide dismutase

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