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Effect of adenosine triphosphate on amiodarone-induced optic neuropathy in rats: biochemical and histopathological
Kemal Bayrakçeken1, Rukiye Kilic Ucgul2, Taha Coban3
1Department of Ophthalmology, Erzincan Binali Yildirim University Faculty of Medicine, Erzincan, Turkey.
Objective:
This study aims to investigate possible preventive effect of ATP on optic nerve damage caused by amiodarone in rats.
Material And Method:
Thirty albino male Wistar rats weighing between 265 and 278 g were used in the study. Before the experiment, the rats were housed at 22 °C in a 12-h light/dark cycle under appropriate condition. The rats were equally divided into five groups of six animals each: healthy group, 50 mg/kg amiodarone (AMD-50), 100 mg/kg amiodarone (AMD-100), 25 mg/kg ATP + 50 mg/kg amiodarone (ATAD-50), and 25 mg/kg ATP + 100 mg/kg amiodarone (ATAD-100). At the end of 14th day, the animals were sacrificed using cardiac puncture under deep thiopental anaesthesia, and optic nerve tissues were harvested to measure superoxide dismutase (SOD), total glutathione (tGSH), malondialdehyde (MDA), and catalase (CAT) levels.
Results:
The MDA levels were found to be significantly higher in the AMD-50 and AMD-100 groups compared to the healthy group (p ˂ 0.001). There was also a significant difference between the AMD-50 and ATAD-50 groups, and between the AMD-100 and ATAD-100 groups regarding MDA levels (p ˂ 0.001). tGSH, SOD, and CAT levels were significantly lower in the AMD-50 and AMD-100 groups compared to the healthy group (p ˂ 0.001). ATP was found to partially inhibit amiodarone-induced optic neuropathy.
Conclusion:
The biochemical and histopathological results of this study demonstrated that amiodarone at high doses caused more severe optic neuropathy inducing oxidative damage, but ATP could relatively antagonise these negative effects on the optic nerve. Therefore, we believe that ATP may be beneficial in preventing amiodarone-induced optic neuropathy.
