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

Physiological Reports

卷:7

Ulrika Widegren¹  Julie Massart¹  Per O. Iversen²  Leonidas S. Lundell³  Emil Kostovski⁴  Mladen Savikj⁴ 

[1] Department of Molecular Medicine and Surgery, Section for Integrative Physiology Karolinska Institutet Stockholm Sweden;

[2] Department of Nutrition, Institute of Basic Medical Sciences University of Oslo Oslo Norway;

[3] Department of Physiology and Pharmacology, Section for Integrative Physiology Karolinska Institutet Stockholm Sweden;

[4] Faculty of Medicine University of Oslo Oslo Norway;

关键词: Atrophy;    oxidative stress;    skeletal muscle;    spinal cord injury;   

DOI  :  10.14814/phy2.14218

来源: DOAJ

【 摘 要 】

Abstract 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.

【 授权许可】

Unknown