title: Neutrophil activation, antioxidant supplements and exercise-induced oxidative stress.
abstract: Neutrophils produce free radicals known as reactive oxygen species (ROS), which assist in the clearance of damaged host tissue. Tissue damage may occur during exercise due to muscle damage, thermal stress and ischaemia/reperfusion. When produced in excess, neutrophil-derived ROS may overwhelm the body's endogenous antioxidant defence mechanisms, and this can lead to oxidative stress. There is increasing evidence for links between oxidative stress and a variety of pathological disorders such as cardiovascular diseases, cancer, chronic inflammatory diseases and post-ischaemic organ injury. A small number of studies have investigated whether there is a link between neutrophil activation and oxidative stress during exercise. In this review, we have summarised the findings of these studies. Exercise promotes the release of neutrophils into the circulation, and some evidence suggests that neutrophils mobilised after exercise have an enhanced capacity to generate some forms of ROS when stimulated in vitro. Neutrophil activation during exercise may challenge endogenous antioxidant defence mechanisms, but does not appear to increase lipid markers of oxidative stress to any significant degree, at least in the circulation. Antioxidant supplements such as N-acetylcysteine are effective at attenuating increases in the capacity of neutrophils to generate ROS when stimulated in vitro, whereas vitamin E reduces tissue infiltration of neutrophils during exercise. Free radicals generated during intense exercise may lead to DNA damage in leukocytes, but it is unknown if this damage is the result of neutrophil activation. Exercise enhances the expression of inducible haem (heme)-oxygenase (HO-1) in neutrophils after exercise, however, it is uncertain whether oxidative stress is the stimulus for this response.
authors.affiliation: School of Human Sciences and Consolidated Research Institute for Advanced Science and Medical Care, Waseda University.
authors.forename: Jonathan
authors.initials: J
authors.lastname: Peake
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Suzuki
mesh_terms: D000111:Acetylcysteine / Q000008:administration & dosage; D000975:Antioxidants / Q000008:administration & dosage* / Q000378:metabolism; D001205:Ascorbic Acid / Q000008:administration & dosage; D004249:DNA Damage; D015444:Exercise / Q000502:physiology*; D006419:Heme Oxygenase (Decyclizing) / Q000097:blood; D051547:Heme Oxygenase-1; D006801:Humans; D066298:In Vitro Techniques; D008565:Membrane Proteins; D018375:Neutrophil Activation / Q000187:drug effects; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D014810:Vitamin E / Q000008:administration & dosage
chemical_list: D000975:Antioxidants; D008565:Membrane Proteins; D017382:Reactive Oxygen Species; D014810:Vitamin E; C496541:HMOX1 protein, human; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1; D001205:Ascorbic Acid; D000111:Acetylcysteine