6533b838fe1ef96bd12a479e
RESEARCH PRODUCT
Role of nuclear factor κB and mitogen-activated protein kinase signaling in exercise-induced antioxidant enzyme adaptation
Jose ViñaJose ViñaLi Li Jil.l. JiLi Li Jil.l. JiMaria-carmen Gomez-cabreram.-c. Gomez-cabreraMaria-carmen Gomez-cabreram.-c. Gomez-cabrerasubject
MAPK/ERK pathwaymedicine.medical_specialtyMAP Kinase Signaling SystemPhysiologyEndocrinology Diabetes and MetabolismBiologymedicine.disease_causeAntioxidantsPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase AExercisechemistry.chemical_classificationReactive oxygen speciesNutrition and DieteticsNF-kappa BSkeletal muscleGeneral MedicineNFKB1EnzymesCell biologyNitric oxide synthasemedicine.anatomical_structureEndocrinologychemistryMitogen-activated protein kinasebiology.proteinMitogen-Activated Protein KinasesOxidative stressdescription
Activation of nuclear factor (NF) κB and mitogen-activated protein kinase (MAPK) pathways in skeletal muscle has been shown to enhance the gene expression of several enzymes that play an important role in maintaining oxidant–antioxidant homeostasis, such as mitochondrial superoxide dismutase (MnSOD) and inducible nitric oxide synthase (iNOS). While an acute bout of exercise activates NFκB and MAPK signaling and upregulates MnSOD and iNOS, administration of chemical agents that suppress reactive oxygen species (ROS) production can cause attenuation of exercise-induced MnSOD and iNOS expression. Thus, ROS generation during exercise may have duel effects: the infliction of oxidative stress and damage, and the stimulation of adaptive responses favoring long-term protection. This scenario explains why animals and humans involved in exercise training have demonstrated increased resistance to oxidative damage under a wide range of physiological and pathological stresses.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2007-10-01 | Applied Physiology, Nutrition, and Metabolism |