Introduction: reactive oxygen species in health and disease

Reactive oxygen species (ROS)—superoxide radicals, hydrogen peroxide and other related compounds—are produced continuously in most tissues. ROS can react with many different macromolecules and thereby cause damage to, for example, DNA, proteins and lipids ([Droge 2002][1]). ROS, therefore, play

[1]  Helmut Acker,et al.  The oxygen sensing signal cascade under the influence of reactive oxygen species , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[2]  M. Duchen,et al.  The role of an astrocytic NADPH oxidase in the neurotoxicity of amyloid beta peptides , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[3]  Min Zhang,et al.  NADPH oxidase-derived reactive oxygen species in cardiac pathophysiology , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[4]  M. Chvanov,et al.  Free radicals and the pancreatic acinar cells: role in physiology and pathology , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[5]  N. Demaurex,et al.  Electron and proton transport by NADPH oxidases , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[6]  Alexei Verkhratsky,et al.  Glucose-sensing neurons of the hypothalamus , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[7]  E. C. Toescu Normal brain ageing: models and mechanisms , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[8]  C. Peers,et al.  A central role for ROS in the functional remodelling of L-type Ca2+ channels by hypoxia , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[9]  L. Tretter,et al.  Alpha-ketoglutarate dehydrogenase: a target and generator of oxidative stress , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[10]  E. Ligeti,et al.  Consequences of the electrogenic function of the phagocytic NADPH oxidase , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[11]  P. Nicotera,et al.  Ca2+ signals and death programmes in neurons , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[12]  T. Godfraind Antioxidant effects and the therapeutic mode of action of calcium channel blockers in hypertension and atherosclerosis , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[13]  W. Dröge Oxidative stress and ageing: is ageing a cysteine deficiency syndrome? , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[14]  M. Jackson Reactive oxygen species and redox-regulation of skeletal muscle adaptations to exercise , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[15]  C. Hidalgo Cross talk between Ca2+ and redox signalling cascades in muscle and neurons through the combined activation of ryanodine receptors/Ca2+ release channels , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[16]  Patrik Rorsman,et al.  Glucose-sensing mechanisms in pancreatic β-cells , 2005, Philosophical Transactions of the Royal Society B: Biological Sciences.

[17]  A. Verkhratsky,et al.  Calcium signalling: past, present and future. , 2005, Cell calcium.

[18]  L. Hunyady,et al.  Control of aldosterone secretion: a model for convergence in cellular signaling pathways. , 2004, Physiological reviews.

[19]  M. Berridge,et al.  Calcium signalling: dynamics, homeostasis and remodelling , 2003, Nature reviews. Molecular cell biology.

[20]  O. Petersen,et al.  Electrophysiology of the pancreas. , 1987, Physiological reviews.

[21]  Alexei Verkhratsky,et al.  Physiology and pathophysiology of the calcium store in the endoplasmic reticulum of neurons. , 2005, Physiological reviews.

[22]  W. Dröge Free radicals in the physiological control of cell function. , 2002, Physiological reviews.