Diabetic neuropathy (DN) is the most common peripheral neuropathy and long-term complication of diabetes. In view of the pathological basis for the treatment of DN, it is important to prevent nerve degeneration. Most of the current treatment strategies are symptomatic therapies. In this study, we evaluated the effectiveness of magnesium-25, carrying porphyrin-fullerene nanoparticles, on diabetes-induced neuropathy. Previous studies have suggested that dorsal root ganglion (DRG) neurons comprise a specific target and may be responsible for the known complications of DN. Experimental DN was induced by intraperitoneal injection of streptozotocin (STZ) (45 mg ⁄ kg). Different forms of magnesium including 25 24 Mg-PMC16 and MgCl 2 were administered intravenously in equal dose (0.5 LD 50 ) at 48-hr intervals before STZ injection. Peripheral nerves were studied after 2 months of diabetes in groups using qualitative approaches, morphometric analysis of DRG neurons and motor function tests. We showed that STZ-induced DN caused morphological abnormalities in DRG neurons comprising changes in area, diameter and number of A and B cells as well as motor dysfunction in DN. Moreover, our findings indicated that administration of 25 Mg-PMC16 as a magnetic form of Mg improved morphological abnormalities and motor dysfunctions significantly, whereas other forms of Mg were ineffective.Diabetic neuropathy (DN) is the most common late complication of diabetes showing an increasing prevalence [1]. Sixty per cent of patients with diabetes show evidence of peripheral nerve disease [2]. Similar to other diabetes complications, DN has been ascribed to hyperglycaemia and subsequent metabolic abnormalities such as increased polyol pathway activity leading to the accumulation of sorbitol and fructose, imbalances in NADP ⁄ NAD + , auto-oxidation of glucose causing the formation of reactive oxygen species, advanced glycation end-products produced by nonenzymatic glycation of proteins, inappropriate activation of protein kinase C (PKC) and a deficit of neurotrophic supports [3]. The pathology of DN includes axonal atrophy, demyelination, loss of nerve fibres and decreased regeneration of nerve fibres [4]. Abnormalities of peripheral nerve function are typical late complications of diabetes. However, by applying streptozotocin (STZ) injections in rats, such a spectrum of disease characteristics can be seen much earlier, i.e. only several weeks after induction of diabetes [5].Based on these observations, pharmacological therapies including aldose reductase inhibitors, antioxidant drugs, aminoguanidine and neurotrophic factors have been used in the treatment of DN [4]. Notwithstanding their importance, these treatments are solely symptomatic therapies, because peripheral nerve tissue damage cannot be reversed. Thus, early diagnosis of DN followed by a stringent pharmacological therapy may be effective to prevent the progression of DN, i.e. arrest the degenerative changes of nerve fibre pathology [4]. Oxidative stress mechanisms by induc...