INTRODUCTION AND OBJECTIVE: Leukemia is a hematological cancer characterized by the exacerbated proliferation of cells of hematopoietic tissue. There are studies showing that the use of cisplatin in patients with leukemia can lead to a satisfactory response in chemotherapy. However, at the beginning of chemotherapy treatment, there may be the development of Tumor Lysis Syndrome due to the large amount of intracellular content from lysis of tumor cells. For this, the treatment of Tumor Lysis Syndrome, carried out in parallel to the chemotherapy treatment, uses a recombinant urate oxidase enzyme. Recombinant urate oxidase is responsible for converting high serum uric acid levels into allantoin, which is more easily eliminated in the urine. However, there are no clinical studies that show the action of allantoin, generated in large quantities, during chemotherapy treatment until its complete elimination by urine. A study by our recently published group shows that allantoin interferes with cisplatin's anti-tumor activity in non-small cell lung cancer cells. Therefore, our objective was to investigate whether allantoin interferes with the action of cisplatin, in vitro, in sensitive chronic myeloid leukemia cells, K562. MATERIAL AND METHOD: Chronic myeloid leukemia cells (K562) were cultured in RPMI 1640 culture medium supplemented with 10% fetal bovine serum, 1% antibiotic, and maintained in an stove at 36°C and 5% CO2. The cells were treated with cisplatin 10 μg / mL and allantoin in different concentrations (25 μg/mL, 50 μg/mL, 100 μg/mL and 200 μg/mL). The cell viability assay was performed using the MTT assay, flow cytometry was used to analyze the induction of DNA fragmentation and the loss of mitochondrial membrane potential was observed by fluorescence microscopy. RESULTS AND CONCLUSION: Our results show that allantoin does not induce cell death in K562 cells and cisplatin leads to decreased viability in K562 cells. However, we observed that in the presence of allantoin there is a reduction in death caused by cisplatin, allowing us to deduce that allantoin enhanced the survival of K562 cells, preventing the efficient action of cisplatin. Since our results show an alteration in the viability of a sensitive leukemia cell, continuing this study, we will simultaneously investigate the effects of allantoin in sensitive and resistant leukemia cells.
Keywords: Allantoin, Leukemia, Cisplatin, Drug Resistance.
Supported by: FAPERJ