Akademik Veri Yönetim Sistemi
Journal of Boron, cilt.10, sa.1, ss.1-9, 2025 (Hakemli Dergi)
This study designed to investigate the biochemical changes in glial cells' oxidant/antioxidant systems in response to glutamate-induced excitotoxicity of boric acid (BA). The present study employed C6 glial cells. For the study, cells were separated into 4 groups as control, glutamate (10mM), glutamate+BA (0,23; 0,46; 0,93; 1,87 and 3,75 μg/mL), and BA (0,23; 0,46; 0,93; 1,87 and 3,75 μg/mL). The control group was not treated. The cells in the glutamate group were treated with 10 mM glutamate for 24 hours. BA was administered one hour prior to the addition of glutamate and incubated for 24 hours. The viability of the cells was evaluated using an XTT assay. Commercial kits were used for biochemical analyses. Significance was set at less than 0.05. The biochemical analysis revealed that the levels of malondialdehyde (MDA), nitric oxide (NO), inducible nitric oxide snythase (iNOS), neuronal nitric oxide synthase (nNOS), and total oxidant status (TOS) were elevated in the glutamate group compared to the control group (p<0.05). It was detemined that BA treatment resulted in a statistically significant reduction in these levels compared to the glutamate group (p<0.05). The levels of SOD and TAS were found to decrease in the glutamate group and to increase with BA pretreatment (p<0.05). The results demonstrated that BA exhibited protective effects on glial cells against glutamate exposure. Furthermore, BA was observed to exert its neuroprotective effect by increasing the antioxidant defense mechanism and reducing oxidative and nitrosative stress.