Altered oxidative stress and antioxidant defence in skeletal muscle during the first year following spinal cord injury

This study investigates how spinal cord injury (SCI) affects oxidative stress, antioxidant capacity, and apoptotic signaling in skeletal muscle during the first year after injury. Oxidative stress, an imbalance between the production and removal of reactive oxygen species (ROS), is known to promote muscle atrophy. The researchers analyzed muscle biopsies from individuals with SCI at 1, 3, and 12 months post-injury, comparing them to able-bodied controls. They measured various markers related to ROS production, antioxidant defenses, and cell death pathways. The results suggest that SCI leads to increased ROS production and apoptosis in the early months after injury, followed by changes in antioxidant capacity and mitochondrial function later on. These findings provide insights into the mechanisms underlying muscle atrophy following SCI.

• 1
  Increased protein content of NADPH oxidase 2, xanthine oxidase, and pro-caspase-3 was observed at 1 and 3 months after spinal cord injury compared to able-bodied controls, suggesting increased ROS production and apoptotic signaling.
• 2
  Total and reduced glutathione content, markers of antioxidant defense, were elevated at 1 and 3 months after SCI, indicating a compensatory response to increased ROS production.
• 3
  At 12 months post-SCI, mitochondrial complexes and superoxide dismutase 2 protein content were decreased, while 4-hydroxynonenal protein adducts (a marker of lipid peroxidation) were increased, suggesting impaired mitochondrial function and increased oxidative damage in the later stages.