Patel Suman, Sinha Ashima, Singh Mahendra Pratap
Industrial Toxicology Research Centre (ITRC), Mahatma Gandhi Marg, Post Box-80, Lucknow-226 001, UP, India.
Neurotoxicol Teratol. 2007 Sep-Oct;29(5):578-85. doi: 10.1016/j.ntt.2007.04.002. Epub 2007 Apr 27.
Behavioral, phenotypic and biochemical changes induced by maneb+paraquat (MB+PQ) in experimental animals have shown their role in the etiologies of Parkinson's disease (PD); however, MB+PQ induced neuronal damage at genome and proteome level have not yet been clearly understood. The present study was undertaken to investigate the differential protein expression patterns in control and MB+PQ treated mouse striatum and to identify differentially expressed proteins. Animals were treated with and without MB+PQ, twice a week for three, six and nine weeks and proteome profiles of striatum were compared. Three differentially expressed proteins were identified as complexin-I, alpha-enolase and glia maturation factor-beta (GMF-beta) using 2D-PAGE and mass spectrometry. The differential expressions were also confirmed at transcription level by semi-quantitative RT-PCR. The results suggest the involvement of complexin-I, alpha-enolase and GMF-beta in MB+PQ induced PD phenotype in mouse.
代森锰锌+百草枯(MB+PQ)在实验动物中诱导的行为、表型和生化变化已表明它们在帕金森病(PD)病因中的作用;然而,MB+PQ在基因组和蛋白质组水平上诱导的神经元损伤尚未完全清楚。本研究旨在调查对照小鼠和经MB+PQ处理的小鼠纹状体中的差异蛋白质表达模式,并鉴定差异表达的蛋白质。对动物进行有无MB+PQ的处理,每周两次,持续三、六和九周,并比较纹状体的蛋白质组图谱。使用二维聚丙烯酰胺凝胶电泳(2D-PAGE)和质谱法鉴定出三种差异表达的蛋白质,分别为突触结合蛋白-I、α-烯醇化酶和神经胶质成熟因子-β(GMF-β)。通过半定量逆转录聚合酶链反应(RT-PCR)在转录水平上也证实了差异表达。结果表明,突触结合蛋白-I、α-烯醇化酶和GMF-β参与了MB+PQ诱导的小鼠PD表型。