Department of Ophthalmology, Erzincan Binali Yildirim University Faculty of Medicine, Erzincan, Turkey.
Department of Ophthalmology, Kirsehir Ahi Evran University Training and Research Hospital, Kirsehir, Turkey.
Cutan Ocul Toxicol. 2023 Sep;42(3):162-167. doi: 10.1080/15569527.2023.2227265. Epub 2023 Jun 27.
This study aims to investigate possible preventive effect of ATP on optic nerve damage caused by amiodarone in rats.
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.
The MDA levels were found to be significantly higher in the AMD-50 and AMD-100 groups compared to the healthy group ( ˂ 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 ( ˂ 0.001). tGSH, SOD, and CAT levels were significantly lower in the AMD-50 and AMD-100 groups compared to the healthy group ( ˂ 0.001). ATP was found to partially inhibit amiodarone-induced optic neuropathy.
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.
本研究旨在探讨三磷酸腺苷（ATP）对胺碘酮致大鼠视神经损伤的可能预防作用。
本研究共使用 30 只雄性白化 Wistar 大鼠，体重 265 至 278 克。实验前，大鼠在 22°C、12 小时光照/黑暗周期的适宜条件下饲养。大鼠被均分为五组，每组 6 只：健康组、50mg/kg 胺碘酮（AMD-50）组、100mg/kg 胺碘酮（AMD-100）组、25mg/kg ATP+50mg/kg 胺碘酮（ATAD-50）组和 25mg/kg ATP+100mg/kg 胺碘酮（ATAD-100）组。第 14 天结束时，大鼠在深度硫喷妥钠麻醉下经心脏穿刺处死，采集视神经组织，以测定超氧化物歧化酶（SOD）、总谷胱甘肽（tGSH）、丙二醛（MDA）和过氧化氢酶（CAT）水平。
与健康组相比，AMD-50 组和 AMD-100 组的 MDA 水平显著升高（P<0.001）。AMD-50 组与 ATAD-50 组、AMD-100 组与 ATAD-100 组之间的 MDA 水平也存在显著差异（P<0.001）。与健康组相比，AMD-50 组和 AMD-100 组的 tGSH、SOD 和 CAT 水平显著降低（P<0.001）。
本研究的生化和组织病理学结果表明，高剂量胺碘酮可引起更严重的视神经病变，诱导氧化损伤，但 ATP 可部分拮抗其对视神经的负面影响。因此，我们认为 ATP 可能有益于预防胺碘酮引起的视神经病变。
