Triphenyltin (IV) Dithiocarbamate Compounds Induce Cytotoxicity in Acute Lymphoblastic Leukemia (Jurkat E6.1) Primarily via DNA Fragmentation and Cell Cycle Arrest

Introduction: A chemotherapeutic agent known as the etoposide is used to treat acute lymphoblastic leukaemia (ALL). Over the years, the etoposide usage in treating ALL has yielded positive outcomes. Nevertheless, it has been discovered that a number of ALL patients experience side-effects and are susceptible to cancer cells. Accordingly, drug research for improved chemotherapy becomes necessary. The results of numerous investigations using compounds containing organotin (IV) dithiocarbamate were encouraging. Aim: The objective of this study is to examine the genotoxicity effects on Jurkat E6.1 cells, derivatives of the aforementioned substances were chosen for this investigation. Materials and Methods: The assessment of cell cycle arrest and genotoxic effects on Jurkat E6.1 cell lines was accomplished using the substances triphenyltin (IV) diisopropyldithiocarbamate (C1) and triphenyltin (IV) dialkyldithiocarbamate (C2). The cell cycle arrest was established using cell cycle analysis. The average DNA tail moment score was used to calculate the genotoxic effects of DNA damage. Inhibitory concentration (IC50) was used to conduct both analyses. C1 has an IC50 of 0.1 M, while C2 has an IC50 of 0.2 M. On the other hand, the etoposide, which served as a positive control, has an IC50 of 0.87 M. Results: The research findings demonstrated that after four hours of treatment, both triphenyltin (IV) dithiocarbamate and etoposide compounds prompted cell cycle arrest, with a significant difference (p < 0.05) in the S phase. Following a four-hour etoposide treatment, the findings of genotoxicity assessment revealed substantial DNA damage (p < 0.05). Furthermore, the C1 and C2 treatments revealed a similar level of DNA damage. However, when a statistical analysis of the comet assay results was accomplished, no discernible change (p > 0.05) was observed. Conclusion: In summary, DNA damage and cell cycle trapping were caused by etoposide, C1, and C2 in Jurkat E6.1 cells.