BACKGROUND CONTEXT Most of the traumatic spinal cord injury (SCI) are treatable, but despite advances in rehabilitation strategies continued impairment in sensorimotor function persists and does not return to pre-injury levels. Following the initial trauma there is a secondary cascade of events characterized by damage to the vasculature of the spinal cord and, therefore, reducing local oxygen delivery to the mitochondria. The main source of ROS (reactive oxygen species; free radicals) production is the mitochondrial electron transport chain. During tissue injury, calcium is released, which activates mitochondrial proteins. The hyperactivate electron transport chain now generates a mitochondrial membrane potential that is above the optimal range. This, in turn, exponentially increases ROS production, which then initiates cellular death cascades causing further damage to the spinal cord, such as inhibiting neuronal differentiation. PURPOSE The purpose of this study was to use a noninvasive infrared red-light therapy (IRL) which reduces the mitochondrial hyperactivity show immediately after SCI. We hypothesized that IRL will reduce mitochondrial hyperactivity which will result in lower ROS production at the epicenter of SCI. METHODS A between-subjects design was used where male Sprague-Dawley rats (3 months old) were randomized into three groups (sham, SCI and SCI + IRL). A balloon catheter model of spinal cord compression was used to induce SCI. The IRL treatment was for 2 hours under anesthesia. RESULTS We found that IRL therapy significantly (p < 0.03) reduced ROS production at the epicenter of SCI. In addition, we found that IL-8 and IL-12 mRNA expression were significantly lower in the SCI + IRL relative to the SCI group, respectively. CONCLUSIONS The results of this pilot study indicated that IRL treatment reduced mitochondrial hyperactivity associated with the initial 24 hours following SCI. FDA DEVICE/DRUG STATUS This abstract does not discuss or include any applicable devices or drugs. Most of the traumatic spinal cord injury (SCI) are treatable, but despite advances in rehabilitation strategies continued impairment in sensorimotor function persists and does not return to pre-injury levels. Following the initial trauma there is a secondary cascade of events characterized by damage to the vasculature of the spinal cord and, therefore, reducing local oxygen delivery to the mitochondria. The main source of ROS (reactive oxygen species; free radicals) production is the mitochondrial electron transport chain. During tissue injury, calcium is released, which activates mitochondrial proteins. The hyperactivate electron transport chain now generates a mitochondrial membrane potential that is above the optimal range. This, in turn, exponentially increases ROS production, which then initiates cellular death cascades causing further damage to the spinal cord, such as inhibiting neuronal differentiation. The purpose of this study was to use a noninvasive infrared red-light therapy (IRL) which reduces the mitochondrial hyperactivity show immediately after SCI. We hypothesized that IRL will reduce mitochondrial hyperactivity which will result in lower ROS production at the epicenter of SCI. A between-subjects design was used where male Sprague-Dawley rats (3 months old) were randomized into three groups (sham, SCI and SCI + IRL). A balloon catheter model of spinal cord compression was used to induce SCI. The IRL treatment was for 2 hours under anesthesia. We found that IRL therapy significantly (p < 0.03) reduced ROS production at the epicenter of SCI. In addition, we found that IL-8 and IL-12 mRNA expression were significantly lower in the SCI + IRL relative to the SCI group, respectively. The results of this pilot study indicated that IRL treatment reduced mitochondrial hyperactivity associated with the initial 24 hours following SCI.