Reactive oxygen species, nutrition, hypoxia and diseases: Problems solved?
Within the last twenty years the view on reactive oxygen species (ROS) has changed; they are no longer only considered to be harmful but also necessary for cellular communication and homeostasis in different organisms ranging from bacteria to mammals. In the latter, ROS were shown to modulate diverse physiological processes including the regulation of growth factor signaling, the hypoxic response, inflammation and the immune response. During the last 60-100 years the life style, at least in the Western world, has changed enormously. This became obvious with an increase in caloric intake, decreased energy expenditure as well as the appearance of alcoholism and smoking; These changes were shown to contribute to generation of ROS which are, at least in part, associated with the occurrence of several chronic diseases like adiposity, atherosclerosis, type II diabetes, and cancer. In this review we discuss aspects and problems on the role of intracellular ROS formation and nutrition with the link to diseases and their problematic therapeutical issues.
Experimental and Molecular Pediatric Cardiology, German Heart Center Munich, Technical University Munich, Germany; DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany.
Agnes
A
Görlach
Faculty of Biochemistry and Molecular Medicine, Biocenter Oulu, University of Oulu, Oulu, Finland.
Elitsa Y
EY
Dimova
Experimental and Molecular Pediatric Cardiology, German Heart Center Munich, Technical University Munich, Germany; DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany.
Andreas
A
Petry
Servicio de Immunología, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa, Madrid, Spain.
Antonio
A
Martínez-Ruiz
Servicio de Immunología, Hospital Universitario de La Princesa, Instituto de Investigación Sanitaria Princesa, Madrid, Spain; Departamento de Bioquímica, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain.
Pablo
P
Hernansanz-Agustín
Department of Life Sciences, University of Coimbra and Center for Neurosciences and Cell Biology, University of Coimbra, Portugal.
Anabela P
AP
Rolo
Department of Life Sciences, University of Coimbra and Center for Neurosciences and Cell Biology, University of Coimbra, Portugal.
Carlos M
CM
Palmeira
Faculty of Biochemistry and Molecular Medicine, Biocenter Oulu, University of Oulu, Oulu, Finland. Electronic address: tkietzm@gwdg.de.
Thomas
T
Kietzmann
D000818:Animals; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D004734:Energy Metabolism / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D000860:Hypoxia / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D029543:Nucleocytoplasmic Transport Proteins / Q000235:genetics / Q000378:metabolism; D009751:Nutritional Requirements / Q000502:physiology*; D009765:Obesity / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress; D011257:Pregnancy Proteins / Q000235:genetics / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction
D016328:NF-kappa B; C038965:NUTF2 protein, human; D029543:Nucleocytoplasmic Transport Proteins; D011257:Pregnancy Proteins; D017382:Reactive Oxygen Species; D020928:Mitogen-Activated Protein Kinases
Diabetes; Diets; Diseases; Free radicals; Hypoxia; Metabolism; Mitochondria; Obesity; Oxygen