Oxidative stress processes

OEHHA Office of Environmental Health Hazard Assessment OSHA Occnpational Safety and Health Administration Osteogenic sarcoma Cancer associated with bone structures Oxidation Chemical addition of oxygen to break down pollutants or organic waste, for example, destruction of chemical substances such as cyanides, phenols, and organic sulfur compounds in sewage by bacterial and chemical means Oxidative stress Process whereby the metabolic balance of a cell is disrupted by exposure to environmental substances, resulting in accumulation of free radicals, which can damage the cell... 

Relatively high occupational Pb exposures clearly induce erythrocyte oxidative stress processes generation of ROS, lipid peroxidation (indexed by MDA levels), and changes in activities of enzymes mediating antioxidant responses (Kasperczyk et al., 2009 Patil et al., 2006 Quintanar-Escorza et al., 2007). One factor operative here may be the potential of ALA accumulation to aid formation of ROS (Ahamad and Siddiqi, 2007). 

FIGURE 6.9 Lewis structure representations of oxygen species involved in oxidative stress processes. Although triplet (ground state) molecular oxygen molecules are sometimes depicted by the simplified Lewis structural formulas shown, a complete description of the electronic behavior of these molecules requires use of molecular orbital theory, which is beyond the scope of this work. 

Figure 23. Artificial muscle formed by a three-layer polypyrrole-nonconducting tape-polypyrrole. The consumed charge works two times in this device when polypyrrole I is oxidized (anodic process), pushing the free end of the layer, polypyrrole II is reduced (cathodic process), trailing the layer. Stresses at the polymer/polymer interfaces are summarized in the box. (Reprinted from Handbook of Organic Conductive Molecules and Polymers, H. S.Nalwa,ed., Vol. 4,1997, Figs. 10.13,10.15a, 10.18,10.36. Reproducedwithpermission of John Wiley Sons, Ltd., Chichester, UK.)...

The protective effects of carotenoids against chronic diseases appear to be correlated to their antioxidant capacities. Indeed, oxidative stress and reactive oxygen species (ROS) formation are at the basis of oxidative processes occurring in cardiovascular incidents, cancers, and ocular diseases. Carotenoids are then able to scavenge free radicals such as singlet molecular oxygen ( O2) and peroxyl radicals particularly, and protect cellular systems from oxidation. 

Although it is widely accepted that ischaemia/ reperfusion-induced oxidant stress is associated with a reduction of Na/K ATPase activity, it is difficult to determine which features of this process are responsible for this effect. A classical approach to this type of problem has been to determine the effect of the application of selected metabolites or agents on the activity of the enzyme of interest, an approach that has been exploited for the sarcolemmal Na/K ATPase and glutathione (Haddock et al., 1990). The application of GSH (O.l-l.OmM) induces a concentration-dependent increase in the activity of a bovine isolated ventricular Na/K ATPase preparation (determined by the ouabain-sensitive hydrolysis of ATP to release inorganic phosphate). In the presence of 1 mM GSH there was a 38% stimulation of activity compared to untreated control... 

If cellular redox state, determined by the glutathione status of the heart, plays a role in the modulation of ion transporter activity in cardiac tissue, it is important to identify possible mechanisms by which these effects are mediated. Protein S-,thiolation is a process that was originally used to describe the formation of adducts of proteins with low molecular thiols such as glutathione (Miller etal., 1990). In view of the significant alterations of cardiac glutathione status (GSH and GSSG) and ion-transporter activity during oxidant stress, the process of S-thiolation may be responsible for modifications of protein structure and function. 

Allopurinol has been shown to attenuate lipid peroxidation in ethanol-fed rats (Kato etal., 1990). However, this was not correlated with any possible effect on histological damage and, as discussed previously, the significance of lipid peroxidation is unclear. Despite the evidence suggesting that oxidative stress and increased oxidative metabolism may play a role in the pathogenesis of human alcoholic liver disease, it remains to be shown that treatment with specific antioxidants will modify this process. 

A second explanation of the ability of oxidative stress to cause DNA damage is that the stress tri ers a series of metabolic events within the cell that lead to activation of nuclease enzymes, which cleave the DNA backbone. Oxidative stress causes rises in intracellular free Ca, which can fiagment DNA by activating Ca -dependent endonucleases (Orrenius etal., 1989 Farber, 1990 Ueda and Shah, 1992) in a mechanism with some of the features of apoptosis (see Wyllie, 1980). An example of apoptosis is the killing of immature thymocytes by glucocorticoid hormones, which activate a cell-destructive process that apparently involves DNA fragmentation by a Ca -dependent nuclease. 

Evans, P.H., Campbell, A.K., Yano, E. and Morgan, L.G. (1989a). Environmental cancer, phagocytic oxidant stress and nutritional interactions. In Nutritional Impact of Food Processing (eds. J.C. Somogyi and H.R. Muller) pp. 313-326. Karger, Basel. 

Variation of the content of impurities in the different CNT preparations [21] offers additional challenges in the accurate and consistent assessment of CNT toxicity. As-produced CNTs generally contain high amounts of catalytic metal particles, such as iron and nickel, used as precursors in their synthesis. The cytotoxicity of high concentrations of these metals is well known [35, 36], mainly due to oxidative stress and induction of inflammatory processes generated by catalytic reactions at the metal particle surface [37]. Another very important contaminant is amorphous carbon, which exhibits comparable biological effects to carbon black or relevant ambient air particles. 

Even in Alzheimer s disease (AD), the possible involvement of a weak excitotoxic process cannot be ruled out. Indeed, mitochondrial abnormalities (such as cytochrome oxidase alterations) [36, 37] and increased levels of markers of oxidative stress [38] have been reported in AD. This has been the rationale for testing the NMDA antagonist memantine in Alzheimer s dementia [39]. 

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