Parkinson’s disease (PD) is caused by progressive neurodegeneration of dopaminergic (DAergic) neurons with abnormal accumulation of α-synuclein in substantia nigra (SN). Studies have suggested the potential involvement of dopamine, iron, calcium, mitochondria and neuroinflammation in contributing to overwhelmed oxidative stress and neurodegeneration in PD. Function studies on PD-causative mutations of SNCA, PRKN, PINK1, DJ-1, LRRK2, FBXO7 and ATP13A2 further indicate the role of oxidative stress in the pathogenesis of PD. Therefore, it is reasonable that molecules involved in oxidative stress, such as DJ-1, coenzyme Q10, uric acid, 8-hydroxy-2’-deoxyguanosin, homocysteine, retinoic acid/carotenes, vitamin E, glutathione peroxidase, superoxide dismutase, xanthine oxidase and products of lipid peroxidation, could be candidate biomarkers for PD. Applications of antioxidants to modulate oxidative stress could be a strategy in treating PD. Although a number of antioxidants, such as creatine, vitamin E, coenzyme Q10, pioglitazone, melatonin and desferrioxamine, have been tested in clinical trials, none of them have demonstrated conclusive evidence to ameliorate the neurodegeneration in PD patients. Difficulties in clinical studies may be caused by the long-standing progression of neurodegeneration, lack of biomarkers for premotor stage of PD and inadequate drug delivery across blood–brain barrier. Solutions for these challenges will be warranted for future studies with novel antioxidative treatment in PD patients.

中文翻译：

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氧化应激在帕金森氏病中的作用。

帕金森氏病（PD）是由多巴胺能（DAergic）神经元进行性神经退行性变性所致，黑质（SN）中的α-突触核蛋白异常蓄积。研究表明，多巴胺，铁，钙，线粒体和神经炎症可能参与了PD的过度氧化应激和神经变性。SNCA，PRKN，PINK1，DJ-1，LRRK2，FBXO7和ATP13A2的PD致病突变的功能研究进一步表明氧化应激在PD的发病机理中的作用。因此，合理的是参与氧化应激的分子，例如DJ-1，辅酶Q10，尿酸，8-羟基-2'-脱氧鸟苷，高半胱氨酸，视黄酸/胡萝卜素，维生素E，谷胱甘肽过氧化物酶，超氧化物歧化酶，黄嘌呤氧化酶和脂质过氧化产物可能是PD的候选生物标志物。应用抗氧化剂调节氧化应激可能是治疗PD的一种策略。尽管已经在临床试验中测试了许多抗氧化剂，例如肌酸，维生素E，辅酶Q10，吡格列酮，褪黑激素和去铁胺，但没有证据表明可以改善PD患者的神经退行性变。神经退行性疾病的长期发展可能会导致临床研究困难，PD运动前期缺乏生物标志物，跨血脑屏障的药物输送不足。这些挑战的解决方案将有待于将来在PD患者中采用新型抗氧化疗法进行研究。