This study has evaluated the action of flavonoid hesperidin on the neurotoxic effects caused by the intake of iron (Fe) in Drosophila melanogaster. Male adult flies, aged 1–3 days, have been divided into four groups of 50 each: (1) control, (2) Hsd 10 μM, (3) Fe 20 mM (4) Hsd 10 μM + Fe 20 mM. During the exposure protocol, the flies have been exposed to a diet containing Hsd and/or Fe for 48 h. The survival and behavioral analyses have been carried out in vivo, and ex vivo. The analyses involved acetylcholinesterase (AChE) activity and Fe levels in the flies' heads and bodies and determination of dopaminergic levels, cellular and mitochondrial viability, activities of superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), reactive species levels (RS), thiobarbituric acid reactive substances (TBARS) and contents of total thiols and non-proteic thiols (NPSH) in the flies' heads. A significant negative correlation between Fe levels in the head of the flies and the survival, dopamine levels and antioxidant enzymes in the head of the flies has been found. Additionally, significant positive correlation between Fe levels in the head of the flies with negative geotaxis RS and AChE activity in the head of the flies has been found. It demonstrates that the flies which had higher levels of Fe in their heads have demonstrated more susceptibility to neurotoxicity. An important result from our study is that Hsd treatment promotes a decrease in Fe concentration in the head, restores dopamine levels and cholinergic activity of the flies and improves motor function caused by Fe. Hsd also ameliorates Fe induced mortality, oxidative stress and mitochondrial dysfunction. Our results have demonstrated the neuroprotective effect of Hsd and it suggests that flavonoid acts in different ways to protect against the Parkinson disease caused by Fe exposure such as the direct scavenging of RS and activation of antioxidant enzymes.

这项研究评估了类黄酮橙皮苷对果蝇中铁（Fe）摄入所引起的神经毒性作用。年龄为1-3天的成年雄性苍蝇分为四组，每组50只：（1）对照，（2）Hsd 10μM，（3）Fe 20 mM（4）Hsd 10μM+ Fe 20 mM。在暴露方案中，将果蝇暴露于含有Hsd和/或Fe的饮食中48小时。生存和行为分析已在体内和离体进行。这些分析涉及果蝇头部和身体中的乙酰胆碱酯酶（AChE）活性和铁水平以及多巴胺能水平，细胞和线粒体活力，超氧化物歧化酶（SOD），过氧化氢酶（CAT），谷胱甘肽-S-转移酶（GST）的活性的测定。 ，蝇头中的反应性物质水平（RS），硫代巴比妥酸反应性物质（TBARS）以及总硫醇和非蛋白硫醇（NPSH）的含量。发现蝇头中的铁水平与蝇头中的存活率，多巴胺水平和抗氧化酶之间存在显着的负相关性。另外，已经发现在具有大地趋向性RS的果蝇头部中的铁水平与果蝇头部中的AChE活性之间存在显着的正相关。这表明在其头部中具有较高Fe含量的果蝇对神经毒性表现出更高的敏感性。我们研究的重要结果是，Hsd处理可促进降低头部的Fe浓度，恢复果蝇的多巴胺水平和胆碱能活性，并改善由Fe引起的运动功能。Hsd还可以改善铁引起的死亡率，氧化应激和线粒体功能障碍。我们的结果证明了Hsd的神经保护作用，它表明类黄酮以不同的方式来预防由铁暴露引起的帕金森氏病，例如直接清除RS和激活抗氧化酶。我们研究的重要结果是，Hsd处理可促进降低头部的Fe浓度，恢复果蝇的多巴胺水平和胆碱能活性，并改善由Fe引起的运动功能。Hsd还可以改善铁引起的死亡率，氧化应激和线粒体功能障碍。我们的结果证明了Hsd的神经保护作用，它表明类黄酮以不同的方式来预防由铁暴露引起的帕金森氏病，例如直接清除RS和激活抗氧化酶。我们研究的重要结果是，Hsd处理可促进降低头部的Fe浓度，恢复果蝇的多巴胺水平和胆碱能活性，并改善由Fe引起的运动功能。Hsd还可以改善铁引起的死亡率，氧化应激和线粒体功能障碍。我们的结果证明了Hsd的神经保护作用，它表明类黄酮以不同的方式来预防由铁暴露引起的帕金森氏病，例如直接清除RS和激活抗氧化酶。