In vitro toxicity of colistin on primary chick cortex neurons and its potential mechanism

Colistin is increasingly used as the last-line therapy for infections caused by Gram-negative superbugs . Although colistin neurotoxicity was reported in the literature, there has no data on its mechanism. In the present study, we examined the effect of colistin on primary chick neuron cells, which were treated with 0.83, 4.15 and 8.3. ?g/mL colistin for 6, 12 and 24. h. Cell viability was evaluated with 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assays after exposure to colistin. Formation of reactive oxygen species (ROS), nuclear morphology, caspase-3 activity and internucleosomal DNA fragmentation were examined. The results showed that, compared with the control, no significant change was observed in cell viability, ROS formation and caspase-3 activity in cells treated for 6, 12 and 24. h with 0.83. ?g/mL colistin. However, in the 4.15 and 8.3. ?g/mL colistin-treated groups, the viability of chick primary neurons significantly decreased at 12 and 24. h, respectively; caspase-3 activities were significantly increased to 5.1 and 7.4 fold at 6. h, more earlier than the changes of ROS, which was significant increased to 124.5 and 143.5 (P