Effect of acrylamide on neurological recovery following spinal cord injuryin rats

Acrylamide (ACR) is a cumulative neurotoxin which causes axonal degeneratio n in animals and man. Industrial workers exposed to ACR have been reported to suffer from a variety of central and peripheral neuropathological sympto ms including numbness of hands and feet, skin peeling and muscular weakness of legs. These reports suggest that the body burden of ACR may be a risk f actor in recovery patterns following neurotrauma. The present study was des igned to assess the effect of ACR on neurological recovery following spinal cord injury (SCI) in rats. Male Sprague-Dawley rats weighing 200-230 g were anaesthetised with chloral hydrate and laminectomy was performed at T 7-8 level leaving the dura inta ct. A compression plate (2.2 x 5.0 mm) loaded with a weight of 35 g was pla ced on the exposed cord for 5 minutes. Animals were divided into seven grou ps of eight rats each. The animals in Group 1 served as control whereas rat s in Group 2 underwent laminectomy alone (sham). The rats in Group 3 to 6 w ere subjected to SCI as mentioned above. Animals in Groups 4, 5 and 6 also received ACR in the doses of 10 mg/kg, 20 mg/kg and 40 mg/kg, i.p., respect ively in addition to SCI, whereas the rats in Group 7 received ACR alone at a dose of 40 mg/kg body weight. The first dose of ACR was given 30 minutes before SCI, followed by daily administration of drug for 7 days. Post trau matic neurological recovery was recorded daily for 10 days using a modified Tarlov score, inclined plane test and sensory and vocal score. Electrophys iological changes were assessed using somatosensory and corticomotor evoked potentials. The animals were sacrificed at different time intervals and th e injured site of the spinal cord was analysed for lipid hydroperoxides (LP H), conjugated dienes (CD) and glutathione (GSH). Neuropathological changes in the spinal cord were assessed using light microscopy. The rats exposed to compression injury alone showed a maximum neurological deficit at 24 hr and then a gradual recovery was observed over a period of 10 days. The rats treated with ACR along with SCI showed poor or no recovery over a period o f 10 days. Our electrophysiological and histopathological studies also conf irmed that concomitant exposure to ACR produces a significant deleterious e ffect on the recovery from SCI. SCI induced increase in oxidative stress (i ncrease in LPH and CD and decrease in GSH) is also exacerbated by ACR sugge sting a role of free radicals. The results of this study suggest that increased body burden of ACR may ret ard the recovery from neurotrauma or even lead to permanent disability.