Protective effects of guanosine on Diazinon induced oxidative stress in neuralgia U373MG cell line
Trauma Monthly: 16 (3); 157-161 Article Type: Research Article
M, Rasooli Vani
J. Protective effects of guanosine on Diazinon induced oxidative stress in neuralgia U373MG cell line,
Online ahead of Print
Aims: Neurologic complications of organophosphates are probably associated with oxidative stress. Guanine derivatives have protective and nutritional effects on astrocytes and other brain cells. In this study the oxidative stress of diazinon and the protective effect guanosine against diazinon on astrocytes cell line types U373MG were evaluated. Materials & Methods: U373MG cells were exposed to different doses of diazinon at different time intervals after culture and the oxidative stress parameters were determined. Then, the protective effects of guanosine on the glutathione level, superoxide dismutase and catalase activity were evaluated. The statistical comparison of different doses of diazinon in different incubation times was done with two-way variance analysis and the comparison of different therapeutic groups was done with one-way variance analysis and Tukey’s post test by Prism software. Results: Diazinon at the dose of 300 μM could significantly decrease the super oxide dismutase and catalase activity 72 hours after exposure. While, either pre- or post-treatment with guanosine could inhibit the glutathione reduction induced by diazinon and increased the glutathione level approximately near the control value, but had no effect on reduction of super oxide dismutase activity. Guanosine pre- or post-treatment increased the catalase activity significantly and could inhibit the reductive effect of diazinon catalase activity. Conclusion: Diazinon is toxic for U373MG cells in a dose and time dependent manner and guanosine could protect cells through the reservation of the glutathione level and catalase activity. These findings indicate that guanosine treatment may induce protective effects against diazinon neuronal toxicity.
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