作者: Wataru Aoi , Yuji Naito , Toshikazu Yoshikawa
DOI: 10.1007/978-94-007-7920-4_15
关键词: Oxidative stress 、 Oxidative phosphorylation 、 Carnitine palmitoyltransferase I 、 Myocyte 、 Reactive oxygen species 、 Biochemistry 、 Skeletal muscle 、 Chemistry 、 Lipid metabolism 、 Mitochondrion
摘要: Exercise leads to the production of reactive oxygen species (ROS) via several sources in skeletal muscle. In particular, mitochondrial electron transport chain muscle cells produces ROS along with an elevation consumption during exercise. Such generated exercise can cause oxidative modification proteins and affect their functionality. Many evidences have been suggested that some proteins, i.e., myofiber metabolic signaling sarcoplasmic reticulum be a targets modified by due We detected carnitine palmitoyltransferase I (CPT I) Ne-(hexanoyl)lysine (HEL), one lipid peroxides, exercised muscles, while antioxidant astaxanthin reduced this stress-induced modification. Exercise-induced may diminish CPT activity caused HEL modification, leading partly limited utilization mitochondria. This protein useful as potential biomarker examine stress levels, compounds, possible benefits