<P> The exact manner in which ROS defends the host from invading microbe is not fully understood . One of the more likely modes of defense is damage to microbial DNA . Studies using Salmonella demonstrated that DNA repair mechanisms were required to resist killing by ROS . More recently, a role for ROS in antiviral defense mechanisms has been demonstrated via Rig - like helicase - 1 and mitochondrial antiviral signaling protein . Increased levels of ROS potentiate signaling through this mitochondria - associated antiviral receptor to activate interferon regulatory factor (IRF) - 3, IRF - 7, and nuclear factor kappa B (NF - κB), resulting in an antiviral state . Respiratory epithelial cells were recently demonstrated to induce mitrochondrial ROS in response to influenza infection . This induction of ROS led to the induction of type III interferon and the induction of an antiviral state, limiting viral replication . In host defense against mycobacteria, ROS play a role, although direct killing is likely not the key mechanism; rather, ROS likely affect ROS - dependent signalling controls, such as cytokine production, autophagy, and granuloma formation . </P> <P> Reactive oxygen species are also implicated in activation, anergy and apoptosis of T cells . </P> <P> In aerobic organisms the energy needed to fuel biological functions is produced in the mitochondria via the electron transport chain . In addition to energy, reactive oxygen species (ROS) with the potential to cause cellular damage are produced . ROS can damage lipid, DNA, RNA, and proteins, which, in theory, contributes to the physiology of aging . </P> <P> ROS are produced as a normal product of cellular metabolism . In particular, one major contributor to oxidative damage is hydrogen peroxide (H O), which is converted from superoxide that leaks from the mitochondria . Catalase and superoxide dismutase ameliorate the damaging effects of hydrogen peroxide and superoxide, respectively, by converting these compounds into oxygen and hydrogen peroxide (which is later converted to water), resulting in the production of benign molecules . However, this conversion is not 100% efficient, and residual peroxides persist in the cell . While ROS are produced as a product of normal cellular functioning, excessive amounts can cause deleterious effects . Memory capabilities decline with age, evident in human degenerative diseases such as Alzheimer's disease, which is accompanied by an accumulation of oxidative damage . Current studies demonstrate that the accumulation of ROS can decrease an organism's fitness because oxidative damage is a contributor to senescence . In particular, the accumulation of oxidative damage may lead to cognitive dysfunction, as demonstrated in a study in which old rats were given mitochondrial metabolites and then given cognitive tests . Results showed that the rats performed better after receiving the metabolites, suggesting that the metabolites reduced oxidative damage and improved mitochondrial function . Accumulating oxidative damage can then affect the efficiency of mitochondria and further increase the rate of ROS production . The accumulation of oxidative damage and its implications for aging depends on the particular tissue type where the damage is occurring . Additional experimental results suggest that oxidative damage is responsible for age - related decline in brain functioning . Older gerbils were found to have higher levels of oxidized protein in comparison to younger gerbils . Treatment of old and young mice with a spin trapping compound caused a decrease in the level of oxidized proteins in older gerbils but did not have an effect on younger gerbils . In addition, older gerbils performed cognitive tasks better during treatment but ceased functional capacity when treatment was discontinued, causing oxidized protein levels to increase . This led researchers to conclude that oxidation of cellular proteins is potentially important for brain function . </P>

Where are reactive oxygen species produced in the body