Özet:

Aim: One of the successful approaches in cancer treatment is the use of specific inhibitors. Responsible for the metabolism of polyunsaturated fatty acids, 12/15-lipoxygenase (12/15-LOX) not only mediates cell death caused by oxidative stress in neurons, but also produces metabolites involved in many important diseases such as cancer. In this study, it was aimed to investigate the anti-proliferative effects of ML351, 12/15-LOX inhibitor, on C6 glioblastoma cells through various biochemical processes. Material and Methods: In the study, cytotoxic ML351 concentrations for C6 cells were determined using methyl thiazolyl tetrazolium (MTT), and then total oxidant capacity (TOS), cytochrome c (CYC), caspase 3 (CASP3), tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) levels were measured. Results: As a result, it was found to have concentration dependent anti-proliferative effects on ML351 C6 cells. It was determined that ML351 treatment increased TOS levels by causing oxidative stress in C6 cells. The ML351 treatment increased CASP3 and CYC levels compared to the control group (p<0.01). Based on these results, it was observed that ML351 treatment induced apoptosis in C6 cells. On the other hand, TNF-α and IL-6 levels were decreased in C6 cells treated with ML351 compared to the control group (p<0.01). Conclusion: Our study shows that ML 351 treatment causes oxidative damage and apoptosis by disrupting the pro-oxidant/oxidant balance and decreases inflammation in C6 glioma cells. Therefore, further studies should be conducted to investigate the effects of ML351, which has the potential to be an anticancer drug, on different metabolic pathways in different cancer cell lines.

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