Awang, N. and Nurul Farahana Kamaludin. 2022 "Cytotoxicity of Diphenyltin(IV) Diisopropyl Dithiocarbamate Compound on Acute Lymphoblastic Leukemia Cells, CCL-119 (CCRF-CEM)" Preprints. https://doi.org/10.20944/preprints202205.0149.v1
Abstract
Acute lymphoblastic leukemia (ALL) is the most common type of leukemia affecting children under the age of 15 years old in Malaysia. Chemotherapy is the primary treatment for cancer, which involves the intake of chemotherapeutic drugs to kill cancer cells. Glucocorticoids such as dexamethasone are chemotherapeutic agents used in the treatment of ALL. Although dexamethasone is highly effective, it is also associated with adverse effects such as bone fractures and organ toxicity. Therefore, there is a need to develop a new anticancer drug which milder side effects and better efficacy. Organometallic compounds such as organotin have a high potential to be developed as an antineoplastic agent and show high specificity towards cancer cells compared to normal cells. This study is done to evaluate the cytotoxic effects of diphenyltin(IV) diisopropyl dithiocarbamate (DPDT) against leukemic cells CCL-119 using the Trypan Blue exclusion (TBE) method at the intervals of 24, 48 and 72 h. Dexamethasone was used as a positive control. The cell’s morphological changes were observed at 12, 24 and 48 h using the IC50 values obtained using TBE assay. Results show that DPDT has a lower IC50 value than dexamethasone against CCL-119 cells at 24 h with a value of 4.16 ± 0.44µM and a selectivity index of 2.02. Dexamethasone exhibited cytotoxic effects against CCL-119 but only IC25 and IC10 values were obtained. Cytotoxicity testing has shown that DPDT is toxic on CCL-119 cells with IC50 values of less than 10µM. Morphological changes in cells show characteristics of apoptosis such as cell shrinkage, blebbing and formation of apoptotic bodies. In conclusion, DPDT has the potential to be made into an antineoplastic agent but requires a more detailed study involving the molecular pathway of DPDT leading to cell death.
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