However, an increasing amount of evidence has shown that mtROS play a more complex role than previously anticipated, actively participating in cellular signaling. Initially ROS were described as simple by-products of metabolism that caused oxidative damage and were responsible for damage upon ischemia-reperfusion or chronic diseases such as Parkinson's or Alzheimer's disease as well as aging ( Sanz et al., 2006). The scientific community has changed its opinion of ROS over the last 15 years.
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Mitochondrial reactive oxygen species (mtROS) produced by the respiratory chain (RC) during oxidative phosphorylation are the main source of free radicals in most cell types. Here, we review what is known about RET, as an example of site-specific ROS signaling, and its implications for the field of redox biology. In Drosophila melanogaster, stimulating RET extends lifespan. RET has been shown to be instrumental for the activation of macrophages in response to bacterial infection, re-organization of the electron transport chain in response to changes in energy supply and adaptation of the carotid body to changes in oxygen levels. This process generates a significant amount of ROS. RET is produced when electrons from ubiquinol are transferred back to respiratory complex I, reducing NAD+ to NADH.
The best example of site-specific ROS signaling is reverse electron transport (RET). However, recent data suggests that the site at which ROS are generated is also instrumental in determining effects on cellular homeostasis. Based on this model the amount of ROS should determine the physiological effect. The current consensus is that low levels of ROS are beneficial, facilitating adaptation to stress via signaling, whereas high levels of ROS are deleterious because they trigger oxidative stress. However, ROS also participate in cellular signaling, are instrumental for several physiological processes and boosting ROS levels in model organisms extends lifespan. Accordingly, mitochondria from old individuals have higher levels of ROS. Reactive Oxygen Species (ROS) can cause oxidative damage and have been proposed to be the main cause of aging and age-related diseases including cancer, diabetes and Parkinson's disease. 2Centro Andaluz de Biología del Desarrollo, Universidad Pablo de Olavide-CSIC and CIBERER-ISCIII, Seville, Spain.1Institute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle University, Newcastle upon Tyne, United Kingdom.
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