enefit of magnesium-25 carrying porphyrin-fullerene nanoparticles in experimental diabetic neuropathy Original Research (7856) Total Article Views Authors: Asieh Hosseini, Mohammad Sharifzadeh, Seyed Mahdi Rezayat, et al Published Date July 2010 Volume 2010:5 Pages 517 - 523 DOI: http://dx.doi.org/10.2147/IJN.S11643 Asieh Hosseini1, Mohammad Sharifzadeh1, Seyed Mahdi Rezayat2, Gholamreza Hassanzadeh3, Shokoufeh Hassani1, Maryam Baeeri1, Vahid Shetab-Bushehri4, Dmitry A Kuznetsov5, Mohammad Abdollahi1 1Faculty of Pharmacy, and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran; 2Faculty of Advanced Science and Technology in Medicine, Tehran University of Medical Sciences and Pharmaceutical Sciences Branch, Islamic Azad University, Tehran, Iran; 3Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran; 4Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran; 5Department of Medicinal Nanobiotechnologies, N. I. Pirogoff Russian State Medical University, Moscow, Russian Federation Abstract: Diabetic neuropathy (DN) is a debilitating disorder occurring in most diabetic patients without a viable treatment yet. The present work examined the protective effect of 25Mg-PMC16 nanoparticle (porphyrin adducts of cyclohexil fullerene-C60) in a rat model of streptozotocin (STZ)-induced DN. 25Mg-PMC16 (0.5 lethal dose50 [LD50]) was administered intravenously in two consecutive days before intraperitoneal injection of STZ (45 mg/kg). 24Mg-PMC16 and MgCl2 were used as controls. Blood 2,3-diphosphoglycerate (2,3-DPG), oxidative stress biomarkers, adenosine triphosphate (ATP) level in dorsal root ganglion (DRG) neurons were determined as biomarkers of DN. Results indicated that 2,3-DPG and ATP decreased whereas oxidative stress increased by induction of DN which all were improved in 25Mg-PMC16-treated animals. No significant changes were observed by administration of 24Mg-PMC16 or MgCl2 in DN rats. It is concluded that in DN, oxidative stress initiates injuries to DRG neurons that finally results in death of neurons whereas administration of 25Mg-PMC16 by release of Mg and increasing ATP acts protectively.