Document Type : Original Article
Authors
1
Department of pharmacology and toxicology, faculty of pharmacy, Egyptian Russian university
2
Department of Pharmacology & Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia 41522, Egypt
3
Pharmacology and Toxicology department, Faculty of Pharmacy, Egyptian Russian University, Cairo, Egypt
4
Pharmacology and Toxicology Department, Faculty of Pharmacy, Suez Canal University, Ismailia, 41522, Egypt.
Abstract
Cisplatin (CP) was recognized as a proficient antineoplastic agent; which has an indispensable role in facing various forms of malignancies such as breast, bladder, cervical, lung, and testicular cancers. Unfortunately, the clinical utilization of CP has faced many obstacles mainly represented in its acquired resistance, and its severe notable toxicities, particularly nephrotoxicity, as well. Despite, the full mechanisms of CP nephrotoxicity are not fully elicited, multiple pathophysiological events have been proposed to define the nephrotoxic effect of CP including accumulation of CP via transport pathway, oxidative stress, inflammation, and apoptosis as well. Importantly, the organic cationic transporter 2 (OCT2) was implicated in the uptake and transportation of CP in to renal cells. Other studies documented the high expression of OCT2 in proximal tubular cells linking it nephrotoxicity induced by CP. This review discusses CP toxicity and its pathophysiology and the role of oxidative stress in the initiation of toxicity in addition to the different therapeutic approaches for its toxicity.
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