Qureshi G Ali, Qureshi Aftab A, Devrajani Bika Ram, Chippa M A, Syed S Ali
Medical Research Centre, Liaquat University of Medical & Health Sciences, Jamshoro, Pakistan.
CNS Neurol Disord Drug Targets. 2008 Feb;7(1):20-7. doi: 10.2174/187152708783885101.
This review deals with the results showing the relation between vitamin B(12) deficiency and neurotoxicity of homocysteine and nitrite (a metabolite of nitric oxide) in Parkinson's patients treated with levodopa (L-Dopa). We have already reported a linear relationship between the CSF levels of nitrite with glutamic acid and homocysteine suggesting that the production of nitrite is interrelated with the neurotoxic level of homocysteine. The levels of nitrite and homocysteine resulting in the deficiency of vitamin B(12) are some of the factors promoting degeneration in Parkinson's disease. This review emphasizes the importance of these parameters in designing suitable drug therapy for Parkinson disease. Additionally, there is evidence that increased homocysteine levels might accelerate dopaminergic cell death in Parkinson disease (PD), through neurotoxic effects. Furthermore, levodopa (L-Dopa) treatment of PD results in hyperhomocysteinemia as a consequence of L-Dopa methylation by catechol-O-methyltransferase (COMT). Therefore, higher dietary intakes of folate, vitamin B12, and vitamin B6 might decrease the risk of PD through decreasing plasma homocysteine.
本综述探讨了左旋多巴（L -多巴）治疗帕金森病患者时，维生素B12缺乏与同型半胱氨酸和亚硝酸盐（一氧化氮的一种代谢产物）神经毒性之间关系的研究结果。我们已经报道了脑脊液中亚硝酸盐水平与谷氨酸和同型半胱氨酸之间的线性关系，这表明亚硝酸盐的产生与同型半胱氨酸的神经毒性水平相互关联。导致维生素B12缺乏的亚硝酸盐和同型半胱氨酸水平是帕金森病中促进神经退行性变的一些因素。本综述强调了这些参数在设计帕金森病合适药物治疗中的重要性。此外，有证据表明，同型半胱氨酸水平升高可能通过神经毒性作用加速帕金森病（PD）中多巴胺能细胞的死亡。此外，左旋多巴（L -多巴）治疗帕金森病会因儿茶酚 - O -甲基转移酶（COMT）对L -多巴的甲基化作用而导致高同型半胱氨酸血症。因此，通过增加饮食中叶酸、维生素B12和维生素B6的摄入量，可能会通过降低血浆同型半胱氨酸水平来降低患帕金森病的风险。
