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Overview
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Background
Cisplatin is a highly effective and broad-spectrum chemotherapeutic agent [1].
Cisplatin is an anticancer agent with some side effects. It is believed to induce apoptosis through several mechanisms. The traditional mechanism is that cisplatin enters the cell, interacts with the DNA guanine bases and forms the inter- or intra-strand chain cross-linking, then prevents the replication of DNA. This formation can also induce apoptosis by activating p53. Cisplatin was also found to cause ROS generation and increase lipid peroxidation, which leads cells to the apoptotic pathway. In addition, cisplatin induces apoptosis with the caspase-dependent pathway. In cochlear cells, cisplatin treatment results in the increase of caspases-3 and -9 and causes the cochlear damage side effect [1].[1] Casares C, Ramírez-Camacho R, Trinidad A, et al. Reactive oxygen species in apoptosis induced by cisplatin: review of physiopathological mechanisms in animal models. European Archives of Oto-Rhino-Laryngology, 2012, 269(12): 2455-2459.
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Overview