Oxidative stress promotes protein degradation and apoptosis in skeletal muscle undergoing atrophy. We aimed to determine whether spinal cord injury leads to changes in oxidative stress, antioxidant capacity, and apoptotic signaling in human skeletal muscle during the first year after spinal cord injury. Vastus lateralis biopsies were obtained from seven individuals 1, 3, and 12 months after spinal cord injury and from seven able-bodied controls. Protein content of enzymes involved in reactive oxygen species production and detoxification, and apoptotic signaling were analyzed by western blot. Protein carbonylation and 4-hydroxynonenal protein adducts were measured as markers of oxidative damage. Glutathione content was determined fluorometrically. Protein content of NADPH oxidase 2, xanthine oxidase, and pro-caspase-3 was increased at 1 and 3 months after spinal cord injury compared to able-bodied controls. Furthermore, total and reduced glutathione content was increased at 1 and 3 months after spinal cord injury. Conversely, mitochondrial complexes and superoxide dismutase 2 protein content were decreased 12 months after spinal cord injury compared to able-bodied controls. In conclusion, we provide indirect evidence of increased reactive oxygen species production and increased apoptotic signaling at 1 and 3 months after spinal cord injury. Concomitant increases in glutathione antioxidant defences may reflect adaptations poised to maintain redox homeostasis in skeletal muscle following spinal cord injury.
Keywords: Atrophy; oxidative stress; skeletal muscle; spinal cord injury.
© 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.