Reactive species in disease: friends or foes?

Abstract This chapter reviews how reactive species (RS) are involved in the origin and progression of human disorders/diseases. This includes atherosclerosis (especially the role of LDL and HDL oxidation), obesity, diabetes (mechanisms of oxidative damage resulting from hyperglycaemia and hyperlipidaemia and how AGE biomolecules form), metabolic syndrome, cystic fibrosis (including oxidative damage caused by P. aeruginosa infection), H. pylori infection, inflammatory bowel diseases (Crohns disease, ulcerative colitis), Dupuytren contracture, Peyronie disease, rheumatoid arthritis, systemic sclerosis, other autoimmune diseases, multiple organ dysfunction syndrome, systemic inflammatory response syndrome, acute respiratory distress syndrome (ARDS), viral infections (especially hepatitis B and C, and HIV), sepsis/septic shock, haemorrhagic shock, anxiety, aneurysm, pancreatitis, chronic pain, coeliac disease, schizophrenia, stress, bipolar disorder, periodontal disease, and adverse drug reactions. The roles of RS in ischaemia–reperfusion (and pre-conditioning) are described, e.g. in stroke, brain trauma, sleep apnoea, claudication, myocardial infarction (including thrombolysis), angioplasty, limb reattachment, and organ transplantation. The roles of RS in the initiation, promotion, and progression of cancer, are presented, especially how RS interact with genes and their products (particularly p53) to drive cancer development. The roles that RS play in carcinogen (e.g. benzopyrene) action, cachexia, and in chemotherapy (e.g. with bleomycin and anthracyclines), and its side-effects are presented. RS formation and antioxidant defences in the healthy and diseased brain and nervous system are explored, especially in Parkinson and Alzheimer diseases, but also in Friedreich ataxia, Huntington disease, multiple sclerosis, amyotrophic lateral sclerosis, amyloid diseases, prions (e.g. Creutzfeldt–Jakob disease), aluminium neurotoxicity, and the neuronal ceroid lipofuscinoses.