Cisplatin has been a mainstay of cancer chemotherapy since the 1970s. Despite its broad anticancer potential, its clinical use has regularly been constrained by kidney toxicities. This review details those biochemical pathways and metabolic conversions that underlie the kidney toxicities. A wide range of redox events contribute to the eventual physiological consequences of drug activities.
Keywords: Alkylating agent; Antioxidants; Bioactivation; Cisplatin; Glutathione; Glutathione S-transferases; Kidney; Nephrotoxicity; Redox pathways; Transporters.
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