Concanavalin A induces apoptosis in a dose-dependent manner by modulating thiol/disulfide homeostasis in C6 glioblastoma cells.

Glioma is the most common brain tumor. C6 rat glioblastoma cells provide thepossibility to the scientist to study brain cancer. Concanavalin A (Con A) has a lot ofantitumoral effects, especially over oxidative stress. In the present study, it wasaimed to decide the impacts of various doses of Con A on C6 glioblastoma cellsregarding cytotoxicity, thiol/disulfide homeostasis, apoptosis, and inflammation. Wedetected the cytotoxic activity of Con A (from 7.8 to 500 µg/ml) in C6 cells byutilizing 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl tetrazolium bromide (MTT) anddetermined the toxic concentration of Con A. Once the optimal doses were found,the thiol–disulfide homeostasis, levels of total antioxidant and oxidant status (TASand TOS), malondialdehyde (MDA) and glutathione (GSH), pro‐inflammatory cytokines as tumor necrosis factor‐alpha (TNF‐α) and interleukin‐6 (IL‐6), apoptoticproteins as cytochrome c (CYCS), and caspase 3 (CASP3) were measured. Apoptoticand morphological changes in the C6 cells were examined with an inverted microscope and flow cytometry technique. Dose‐dependent Con A triggered oxidativedamage in the C6 cells, affecting the inflammatory pathway, so reducing proliferation with apoptotic proteins and morphological changes. But especially, Con A increased disulfide formation by disrupting the thiol/disulfide balance in C6 cells. Thisstudy revealed that Con A, known as carbohydrate‐binding protein, generatedoxidative damage, inflammation, and apoptosis in a dose‐dependent manner bymodulating thiol/disulfide homeostasis in C6 glioblastoma cells.