For Health Professionals

Oxidative stress is defined as an imbalance between the formation and elimination of so-called reactive oxygen species (ROS). They are formed when oxygen utilisation is uncoupled from its metabolic use. ROS have been suggested as major disease triggers. The concept is very popular and easy to understand, which has lead to a widespread use of antioxidant vitamins by patients with a variety of diseases and by healthy people to improve wellbeing. Indeed, up to half of the population in high-income countries use vitamins supplements, often marketed as antioxidants. However, clinical trials showed that untargeted application of antioxidants, which broadly scavenge ROS, are not only ineffective but may even be harmful. As a result, no antioxidant has ever been approved by a regulatory agency, and their use is confined to alternative medicine and uncontrolled self-prescription. One likely reason why antioxidant supplements do not work is the double-edged role of ROS. They are not only ‘bad’ disease mediators causing tissue damage, but are also essential signalling molecules. Thus, similar to an excess (‘oxidative stress’), a deficiency in ROS results in a redox imbalance (in this case harmful ‘reductive stress’).

ROS and their (patho-)physiological roles have been intensely studied for many years with, however, little public impact: The consumers’ belief in the health benefits of antioxidants is still powerful. Therefore, EU-ROS will move away from the antioxidant concept, both scientifically and with respect to public awareness. Rather, EU-ROS aims to identify and then modulate disease-relevant molecular sources of excess ROS, leaving those sources of ROS intact that are essential for adaptation and physiologic signalling. EU-ROS also aims to revert molecular damage caused by oxidative stress. This will be complemented by the development of evidence-based biomarkers and novel imaging technologies. Finally, EU-ROS will elucidate those cases in which antioxidants – in the correct combinations, form, doses and duration – may be useful.

Inflammatory cells, vascular dysfunction and atherothrombosis. The scheme illustrates the activation of immune cells and recruitment to vascular tissues leading to activation of secondary RONS sources such as NADPH oxidase and uncoupled eNOS, all of which contributes to vascular dysfunction. These processes lead to late-stage cardiovascular complication such as atherosclerosis with plaque formation and thrombosis. Vice versa, vascular RONS can activate immune cells and Trigger their Infiltration into the vascular wall. From Karbach et al. Curr. Pharm. Des. 2014. With permission of Bentham Science Publishers.

Inflammatory cells, vascular dysfunction and atherothrombosis. The scheme illustrates the activation of immune cells and recruitment to vascular tissues leading to activation of secondary RONS sources such as NADPH oxidase and uncoupled eNOS, all of which contributes to vascular dysfunction. These processes lead to late-stage cardiovascular complication such as atherosclerosis with plaque formation and thrombosis. Vice versa, vascular RONS can activate immune cells and Trigger their Infiltration into the vascular wall. From Karbach et al. Curr. Pharm. Des. 2014. With permission of Bentham Science Publishers.

Mechanisms of endothelial and smooth muscle dysfunction with special emphasis on redox processes and oxidative stress for known cardiovascular risk factors. Potential targets of pharmacological compounds to suppress oxidative stress and progression of the disease or cardiovascular complications. Karbach et al. Curr. Pharm. Des 2014. With permission of Bentham Science Publishers.

Mechanisms of endothelial and smooth muscle dysfunction with special emphasis on redox processes and oxidative stress for known cardiovascular risk factors. Potential targets of pharmacological compounds to suppress oxidative stress and progression of the disease or cardiovascular complications. Karbach et al. Curr. Pharm. Des 2014. With permission of Bentham Science Publishers.