Role of ROS and RNS Sources in Physiological and Pathological Conditions

Abstract

There is significant evidence that, in living systems, free radicals and other reactive oxygen and nitrogen species play a double role, because they can cause oxidative damage and tissue dysfunction and serve as molecular signals activating stress responses that are beneficial to the organism. Mitochondria have been thought to both play a major role in tissue oxidative damage and dysfunction and provide protection against excessive tissue dysfunction through several mechanisms, including stimulation of opening of permeability transition pores. Until recently, the functional significance of ROS sources different from mitochondria has received lesser attention. However, the most recent data, besides confirming the mitochondrial role in tissue oxidative stress and protection, show interplay between mitochondria and other ROS cellular sources, so that activation of one can lead to activation of other sources. Thus, it is currently accepted that in various conditions all cellular sources of ROS provide significant contribution to processes that oxidatively damage tissues and assure their survival, through mechanisms such as autophagy and apoptosis.

Rapamycin Protects Skin Fibroblasts from Ultraviolet B-Induced Photoaging by Suppressing the Production of Reactive Oxygen Species

“…Di et al reported that UVB irradiation generated first stage intracellular ROS, such as superoxide radical anions (O 2 -), H 2 O 2 , and hydroxyl radicals (-OH), either directly or through enzyme activation [48]. Based on our results, we propose that the anti-aging mechanism of RAPA occurs by decreasing ROS accumulation and thus increasing the autophagy level.…”

Anthocyanidins and anthocyanins: colored pigments as food, pharmaceutical ingredients, and the potential health benefits

“…ROS and RNS are generated in several cellular systems in the human body. ROS is typically produced in cytosol, mitochondrial, peroxisomes, endoplasmic reticulum, plasma membrane, and lysosomes, whereas RNS is produced from amino acid metabolism [141]. …”

“…At the Complexes I and III in mitochondrial, hydroxyl radical (•OH) is generated via a Fenton reaction (H 2 O 2 + Fe 2+ → •OH + OH− + Fe 3+ ). There are other pathways involved in the production of ROS (O 2 •− ), such as through a α-ketoglutarate dehydrogenase complex and by several oxidoreductases in the mitochondrial [141]. A similar mechanism of action also occurs in peroxisomes and lysosomes, which involves metabolism of H 2 O 2 .…”

Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

“…Indeed, various processes occurring in mitochondria and other cellular sites, including cytosol, endoplasmic reticulum, peroxisomes and lysosomes (Venditti et al 2015, Di Meo et al 2016, lead to partial oxygen reduction and formation of free radicals and other reactive oxygen species (ROS). ROS include superoxide anion radical (O 2…”

“…Similarly, mitochondrial ROS production is thought to both play a major role in tissue oxidative damage and dysfunction and provide protection against excessive tissue dysfunction (Venditti & Di Meo 2006), even though it is apparent that in various conditions remarkable contribution to tissue oxidative stress and protection is provided by other sources of ROS and RNS (Di Meo et al 2016). The issue is complicated by the strong interaction existing among the various cellular sources of ROS (Camões et al 2009, Vannuvel et al 2013, which makes it difficult to establish what source of reactive species plays a prominent role in different physiological and pathological conditions.…”