Diaz-Ruiz Araceli, Alcaraz-Zubeldia Mireya, Maldonado Valente, Salgado-Ceballos Hermelinda, Mendez-Armenta Marisela, Rios Camilo
Departamento de Neuroquímica, Instituto Nacional de Neurologia y Neurocirugia Manuel Velasco Suarez S.S.A., Mexico.
Neurosci Lett. 2009 Mar 6;452(1):56-9. doi: 10.1016/j.neulet.2009.01.020. Epub 2009 Jan 13.
Spinal cord injury (SCI) is a world-wide health problem. After traumatic injury, spinal cord tissue starts a series of self-destructive mechanisms, known as the secondary lesion. The leading mechanisms of damage after SCI are excitotoxicity, free radicals' overproduction, inflammation and apoptosis. Metallothionein (MT) and reduced glutathione (GSH) are low-molecular-weight, cysteine-rich peptides able to scavenge free radicals. MT and GSH participation as neuroprotective molecules after SCI is unknown. The aim of the present study is to describe the changes of MT and GSH contents and GSH peroxidase (GPx) activity in the acute phase after SCI in rats. Female Wistar rats weighing 200-250g were submitted to spinal cord contusion model, by means of a computer-controlled device (NYU impactor). Rats receiving laminectomy were used as a control group. Animals were killed 2, 4, 12 and 24h after surgery. MT was quantified by the silver-saturation method, using atomic absorption spectrophotometry. GSH and GPx were assayed by spectrophotometry. Results indicate an increased MT content by effect of SCI, only at 4 and 24h, as compared to sham group values. Meanwhile, GSH was found decreased at 4, 12 and 24h after SCI. Interestingly, GPx activity was raised at all time points, indicating that this enzymatic defense is activated soon after SCI. Results suggest that thiol-based defenses, MT and GSH, are differentially expressed by spinal cord tissue to cope with the various processes of damage after lesion.
脊髓损伤（SCI）是一个全球性的健康问题。创伤性损伤后，脊髓组织会启动一系列自我破坏机制，即所谓的继发性损伤。脊髓损伤后主要的损伤机制包括兴奋性毒性、自由基过量产生、炎症和细胞凋亡。金属硫蛋白（MT）和还原型谷胱甘肽（GSH）是低分子量、富含半胱氨酸的肽，能够清除自由基。SCI后MT和GSH作为神经保护分子的参与情况尚不清楚。本研究的目的是描述大鼠SCI急性期MT和GSH含量以及GSH过氧化物酶（GPx）活性的变化。体重200 - 250g的雌性Wistar大鼠通过计算机控制装置（纽约大学撞击器）建立脊髓挫伤模型。接受椎板切除术的大鼠作为对照组。术后2、4、12和24小时处死动物。采用原子吸收分光光度法通过银饱和法对MT进行定量。通过分光光度法测定GSH和GPx。结果表明，与假手术组相比，SCI仅在4小时和24小时时导致MT含量增加。同时，发现SCI后4、12和24小时GSH含量降低。有趣的是，GPx活性在所有时间点均升高，表明这种酶促防御在SCI后很快被激活。结果表明，基于硫醇的防御物质MT和GSH在脊髓组织中差异表达，以应对损伤后的各种损伤过程。
