In a study involving melanoma-bearing mice, Cisplatin administration (4 mg/kg B.W.) effectively reduced the size and weight of solid tumors. Moreover, supplementing Cisplatin treatment with HemoHIM further decreased both tumor size and weight, highlighting a potential synergistic effect^[3].

Cisplatin treatment also results in notable adverse effects on kidney function, as demonstrated in a study where its administration significantly increased kidney weight as a percentage of total body weight, urine volume, serum creatinine, and blood urea nitrogen levels by approximately 132, 315, 797, and 556%, respectively, compared to control rats^[4].

When applied to HeLa cells, Cisplatin induces apoptosis in a dose-dependent manner, with a 30 μM concentration leading to the death of over 90% of the cells within 24 hours of treatment. Investigations into the kinetics of Cisplatin-induced apoptosis at this concentration have revealed that it activates the MEK/ERK signaling pathway. Notably, both 20 and 30 μM concentrations of Cisplatin significantly induce apoptosis and lead to a robust activation of ERK^[1].

Cisplatin, at a 50 μM concentration, induces apoptosis in renal proximal tubular cells (RPTCs) in a time-dependent manner. This process is marked by cellular shrinkage, a 50-fold increase in caspase 3 activity, a fourfold rise in phosphatidylserine externalization, and significant increases in chromatin condensation and DNA hypoploidy by 5- and 15-fold, respectively^[2].