The term Reactive Oxygen Species (ROS) describes several reactive molecules and free radicals derived from molecular oxygen. The production of oxygen-based radicals is the bane of all aerobic species. These molecules, produced as byproducts during the mitochondrial electron transport of aerobic respiration or by oxidoreductase enzymes and metal-catalyzed oxidation, can potentially cause several deleterious events. It was initially thought that only phagocytic cells were responsible for ROS production as part of host cell defense mechanisms. Recent work has demonstrated that ROS has a role in cell signaling, including apoptosis, gene expression, and the activation of cell signaling cascades. It should be noted that ROS can serve as both intra- and intercellular messengers.
Detoxification of reactive oxygen species is paramount to the survival of all aerobic life forms. As such, several defense mechanisms have evolved to meet this need and provide a balance between the production and removal of ROS. An imbalance toward the pro-oxidative state is often called “Oxidative stress.”
Cells have a variety of defense mechanisms to ameliorate the harmful effects of ROS. Superoxide dismutase (SOD) catalyzes the conversion of two superoxide anions into a molecule of hydrogen peroxide (H2O2) and oxygen (O2). In the peroxisomes of eukaryotic cells, the enzyme catalase converts H2O2 to water and oxygen and thus completes the detoxification initiated by SOD. Glutathione peroxidase is a group of enzymes containing selenium, which also catalyzes the degradation of hydrogen peroxide and organic peroxides to alcohols.
Several non-enzymatic small-molecule antioxidants play a role in detoxification. Glutathione may be the most important intracellular defense against the deleterious effects of reactive oxygen species. Vitamin C, or ascorbic acid, is a water-soluble molecule capable of reducing ROS, while vitamin E (α-tocopherol) is a lipid-soluble molecule that has been suggested as playing a similar role in membranes.
ROS and Diseases
Researchers have been trying to elucidate ROS's mechanisms and role in diseases since they were identified. ROS influences diseases mainly through its function as signaling molecules and oxidants that affect cell survival and oxidative damage. ROS could also drive immunity through immunological defense and maintain metabolic balance or heat dissolving.
ROS can function as intermediates in varying pathways, but they are also widely regarded as etiologic factors for diseases, including cancer, inflammation, and organ injuries. Evidence suggests that the scavenging ROS in pathological conditions may reduce cell damage and control the pathological process.
The ROS have both positive and negative impacts on various diseases:
- Cancer positive impact: Impair tumorigenesis, apoptosis
- Cancer negative impact: High metastasis, canceration, radioresistance, carcinogenesis
- Inflammatory diseases' positive impact: Prevent experimental autoimmune encephalomyelitis, support the immune system, macrophage killing
- Inflammatory diseases' negative impact: Inflammatory bowel diseases, parasite-caused organic damage, periodontitis, tendinopathy, bronchitis, emphysema, rheumatoid arthritis
- Neurologic diseases' positive impact: Synaptic plasticity, neuronal development
- Neurologic diseases' negative impact: Movement disorder, neuron apoptosis, neurotoxicity, retardation
- Vascular diseases' positive impact: Relaxation of cerebral arteries, blood flow homeostasis, wound repair
- Vascular diseases negative impact: Hypertension, vascular injury, ischemia-reperfusion damage, retinal dysfunction, pneumoconiosis, atherosclerosis, acute respiratory distress syndrome
- Organ failure positive impact: Respiratory plasticity, sensory plasticity
- Organ failure negative impact: Liver failure, renal failure, heart failure
- Diabetes negative impact: Insulin resistance
- Aging positive impact: Muscle cell development, muscle remodeling
- Aging negative impact: Sarcopenia, muscular dystrophy, DNA damage
- Infertility's negative impact: Damage to spermatogenesis, ovarian toxicity
