Cisplatin (CDDP) is an antineoplastic chemotherapy agent by cross-linking with DNA and causing DNA damage in cancer cells. Cisplatin activates ferroptosis and induces autophagy^[1][2][3]. IC50 & Target: DNA Alkylator/Crosslinker^[1] In Vitro: Cisplatin (CDDP) causes apoptosis of HeLa cells in a dose-dependent manner, with a concentration of 30 μM Cisplatin resulting in death of greater than 90% of the cell population by 24 h of treatment. The kinetics of Cisplatin-induced apoptosis are examined using a 30 μM concentration. Cisplatin Activates the MEK/ERK Signaling Pathway, 20 and 30 μM Cisplatin, both of which results in significant apoptosis, leads to strong activation of ERK^[1].
Cisplatin (50 μM) produces time-dependent apoptosis in renal proximal tubular cell (RPTCs), causing cell shrinkage, a 50-fold increase in caspase 3 activity, a 4-fold increase in phosphatidylserine externalization, and 5- and 15-fold increases in chromatin condensation and DNA hypoploidy, respectively^[2]. In Vivo: In melanoma-bearing mice, Cisplatin (CDDP; 4 mg/kg B.W.) reduces the size and weight of the solid tumors, and HemoHIM supplementation with Cisplatin enhances the decrease of both the tumor size and weight^[3].
Cisplatin administration results in significant increases in the kidney weight as a percentage of the total body weight, urine volume, serum creatinine, and blood urea nitrogen by about 132, 315, 797, and 556% in comparison with the control rats, respectively^[4].