Olanow C W
Department of Neurology, University of South Florida, Tampa 33606.
Neurology. 1990 Oct;40(10 Suppl 3):suppl 32-7; discussion 37-9.
Free radicals generated from oxidation reactions may contribute to the pathogenesis of Parkinson's disease (PD). Free radicals are capable of reacting almost instantaneously with membrane lipids and causing lipid peroxidation, membrane injury, and cell death. Dopamine is metabolized by oxidation reactions capable of generating free radicals. Recent evidence indicates that the substantia nigra of patients with PD contains increased iron, which enhances oxidation, and decreased glutathione, which protects against the formation of free radicals. Further, the end products of lipid peroxidation are increased in the substantia nigra of patients with PD, supporting the notions that free radicals are being generated and may contribute to dopamine neuronal death. This hypothesis suggests that antioxidant therapies may slow the rate of progression of PD and raises concern that metabolites of levodopa therapy may accelerate the rate of neuronal degeneration.
氧化反应产生的自由基可能在帕金森病(PD)的发病机制中起作用。自由基能够几乎瞬间与膜脂质发生反应,导致脂质过氧化、膜损伤和细胞死亡。多巴胺通过能够产生自由基的氧化反应进行代谢。最近的证据表明,帕金森病患者的黑质中铁含量增加,这会增强氧化作用,而谷胱甘肽含量降低,谷胱甘肽可防止自由基的形成。此外,帕金森病患者黑质中脂质过氧化的终产物增加,这支持了自由基正在产生且可能导致多巴胺神经元死亡的观点。这一假说表明,抗氧化疗法可能会减缓帕金森病的进展速度,并引发人们对左旋多巴治疗的代谢产物可能加速神经元变性速度的担忧。