Silicon Dioxide Nanoparticles (SiO2, 40-50 nm) Exacerbate Pathophysiology of Traumatic Spinal Cord Injury and Deteriorate Functional Outcome in the Rat. An Experimental Study Using Pharmacological and Morphological Approaches

Silicon (SiO(2)) nanoparticles or silica dust is quite common form of exposure to soldiers engaged in gulf war that may influence their health and brain function. It is quite likely that traumatic injuries to the CNS may be influenced by exposure to these nanoparticles. However, the details of silicon nanoparticles on human health functions are still unknown. In this investigation we examined the effects of chronic silicon dioxide nanoparticles (SiO(2), 40-50 nm) exposure on spinal cord injury (SCI) induced alterations on the functional outcome and the cord pathology in a rat model. Since nanciparticles induce oxidative stress, the influence of an antioxidant compound H-290/51 was also examined in these nanoparticles treated injured rats as well. Rats treated with SiO(2) for 7 days did not show any significant alteration in behaviour on rota rod performances or on capacity angle tests. However, subjection of these nanciparticles exposed rats to SCI resulted in a profound deterioration in motor functions compared to normal rats with SCI. The magnitude of blood-spinal cord barrier (BSCB) disruption to Evans blue and radioiodine tracers and edema formation was much more aggravated following SCI in nanoparticles treated animals compared to untreated traumatized rats. Pretreatment with H-290/51 (50 mg/kg, p.o.) 30 min before SCI in nanoparticle treated rats did not alter spinal cord pathology or functional outcome, however, this dose of the compound was very effective in reducing pathophysiology of SCI in normal animals. These observations are the first to suggest that exposure of nanoparticles enhances the sensitivity of CNS to injuries and alter the effect of neuroprotective drugs.