Reactive oxygen species toxicity

S. Magder, Reactive oxygen species toxic molecules or spark of life Crit. Care 10, 208 (2006)... 

One of the important consequences of neuronal stimulation is increased neuronal aerobic metabolism which produces reactive oxygen species (ROS). ROS can oxidize several biomoiecules (carbohydrates, DNA, lipids, and proteins). Thus, even oxygen, which is essential for aerobic life, may be potentially toxic to cells. Addition of one electron to molecular oxygen (O,) generates a free radical [O2)) the superoxide anion. This is converted through activation of an enzyme, superoxide dismurase, to hydrogen peroxide (H-iO,), which is, in turn, the source of the hydroxyl radical (OH). Usually catalase... 

Bronchial Asthma. Figure 2 Mechanisms of bronchial hyperresponsiveness. Toxic products from eosinophils [cationic peptides, reactive oxygen species (ROS)] cause epithelial injury. Nerve endings become easily accessible to mediators from mast cells, eosinophils [eosinophil-derived neurotoxin (EDN)], and neutrophils, and to airborne toxicants such as S02. Activation of nerve endings stimulates effector cells like mucosal glands and airway smooth muscle either directly or by cholinergic reflexes. 

This situation may be about to change as we look at the role of iron and its implications in the formation of reactive oxygen species, with their potential to attack, modify, and ultimately destroy cells. The signalling function of ROS, not to mention RNS, has been underlined earlier. Yet, we tread a delicate, and poorly understood balance between low levels of ROS, required both for cell signalling and to maintain the antioxidative defences of the cell in a state of alert1"1, and levels which become toxic. This remains an extremely important area of therapeutic concern, since oxidative stress, whether proven to be due to iron or not, is... 

Fig. 2 Possible mechanisms by which nanoparticles cause toxicity inside cells. GSH glutathione, GSSG glutathione disulfide, MDA malondialdehyde, NFkB nuclear factor kappa B, Nrf2 nuclear factor-erythroid 2-related factor 2, ROS reactive oxygen species...

The use of hydrogen peroxide as an oxidant is not compatible with the operation of a biocatalytic fuel cell in vivo, because of low levels of peroxide available, and the toxicity associated with this reactive oxygen species. In addition peroxide reduction cannot be used in a membraneless system as it could well be oxidized at the anode. Nevertheless, some elegant approaches to biocatalytic fuel cell electrode configuration have been demonstrated using peroxidases as the biocatalyst and will be briefly reviewed here. 

As the superoxide radical is a precursor of the other reactive oxygen species and interacts with blood plasma components under physiological and pathological conditions as well, systems related to its generation are biologically relevant. It should be noted, however, that with respect to the initiation of lipid peroxidation as one of the main causes of oxidative cell damage, its own reactivity is very weak and that only in protonized form is its toxicity comparable to that of lipid peroxyl radicals [18]. 

General descriptors may be related to the metabolism responses in the biofilm. Biofilm algae have several mechanisms to counterbalance the damage caused by the toxicants. Environmental stress produces oxidative damage in the cells, which can be tracked down by means of the analysis of many enzymes (superoxide dismutase, catalase, peroxidase, etc.) that function as effective quenchers of reactive oxygen species (ROS). 

Reactive oxygen species may modify both the excito-toxic and the apoptotic components of ischemic brain damage. In addition to direct effects of oxidative injury during ischemia-reperfusion, ROS may modify ischemic excitotoxicity by downregulating current through NMDA receptors. However, exposure to oxidative stress can be... 

The toxicity of C60 has been found to be related to its ability to cause oxidative stress (Oberdorster, 2004 and Sayes et al., 2005, 2007). However, literature describing the toxicity of C60 is contradictoiy. The first report on C60 cytotoxicity originated from Tsuchiya et al. who found that C60 inhibited cell proliferation and differentiation dose-dependently in mouse midbrain cells treated at -400 pg/ml for six days. Tsuchiya et al. proposed that reactive oxygen species (ROS) contributed to C60 cytotoxicity. The ROS generation and embryo head abnormalities suggested that C60 may contribute to brain and neuronal diseases such as Down syndrome, Alzheimer s, and Parkinson s disease (Tsuchaiya, 1996). The research that... 

Pulskamp K, Diabate S, Krug HF (2007). Carbon nanotubes show no sign of acute toxicity but induce intracellular reactive oxygen species in dependence on contaminants. Toxicol. Lett. 168(1) 58-74. 

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