Oxidants, injurious

Stress Heat-fever Heavy metals Oxidant injury Oxidative uncouplers Ischemia... 

As more is learned about the chromosomal effects on HS gene expression, it is important to point out that these genes are actually a subset of inducible responses to cellular stress. Not all of these inducible responses involve HSF, and this indicates that cells have diversified transcriptional responses to cope with different types of stress. This diversification is manifested by glucose regulated genes (grp), as well as the metallothionein and oxidant-injury genes (Watswich, 1988 Storz et al., 1990 Devary et al., 1992 Skroch et al., 1993 Xu, 1993). 

Kurashige, M. et al., Inhibition of oxidative injury of biological membranes by astaxanthin. Physiol. Chem. Phys. Med. NMR, 22, 27, 1990. 

Ueda, N. and Shah, S.V. (1992). Endonuclease-induced DNA damage and cell death in oxidant injury to renal tubular epithelial cells. J. Clin. Invest. 90, 2593-2597. 

Yeadon, M., Darley-Usmar, V., Payne, A. N. (1991a). Mechanism of oxidant injury in isolated, perfused, ventilated guinea-pig lungs induced by hydrogen peroxide. Am. Rev. Resp. Dis. 143, A581. 

Simon, L.M. and Suttorp, N. (1983). Lung cell oxidant injury decrease in polymorphonuclear leucocyte mediated cytotoxicity by N-acetyl cysteine. Am. Rev. Resp. Dis. 127, 286. 

HOCl is one of the oxidants that activated phagocytes have in their arsenal. Hu et al. (1993) have shown that plasma albumin sulphydryl and ascorbic acid both protect against oxidant injury from HOCl. Neutrophils, interestingly, contain about 25 times more ascorbic acid than plasma. This su ests an endogenous self-protection role. This work is important because of the biological emphasis of reactive chlorine by the neutrophil. 

Sala, R., Moriggi, E., Corvasce, G. and Morelli, D. (1993). Protection by N-acetylcysteine a iinst pulmonary endothelial cell damage induced by oxidant injury. Eur. Respir. J. 6, 440-446. 

Expression of matrix metalloproteinases (MMPs) and their inhibitors is an important function of the RPE, particularly with respect to the maintenance of appropriate permeability of the Bruch s membrane (Ahir et al., 2002). This function can be tested in vitro (Marin-Castano et al., 2006). For example, it has been shown that the expression of MMP-2, TIPM-2s (tissue inhibitor of MMP-2), and type IV collagen by cultured ARPE-19 cells is affected by repetitive exposures to nonlethal oxidant injury with hydroquinone (Marin-Castano et al., 2006). Oxidative stress decreases MMP-2 activity and increases collagen type IV accumulation. 

Marin-Castano, ME, Striker, GE, Alcazar, O, Catanuto, P, Espinosa-Heidmann, DG, and Cousins, SW, 2006. Repetitive nonlethal oxidant injury to retinal pigment epithelium decreased extracellular matrix turnover in vitro and induced sub-RPE deposits in vivo. Invest Ophthalmol Vis Sci 47,4098-4112. 

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... 

NO has complex roles in immunological host responses against viruses, and especially against HIV-1 infection. In HIV-1 infection, NO cannot be rigidly classified as an anti-inflammatory or proinflammatory molecule, but it can be deemed a true inflammatory mediator. Many studies support a proviral effect of NO in HIV-1 infection, mainly based on stimulation of viral replication, and on toxic effects on various cells, including central nervous system cells, via oxidative injury that may cause cellular and organ dysfunction, and immunosuppression and immunopathology, especially in the central nervous system. 

Messana, J.M., Cieslinski, D.A., O Connor, R.P. and Humes, H.D. (1988). Glutathione protects against exogenous oxidant injury to rabbit renal proximal tubules. Amer. J. Physiol. 255 F874-F884. 

In single dose oral studies with rats, endrin treatment was associated with an increased incidence (2.4-3.5-fold) in the number of DNA single strand breaks in hepatocytes (Bagchi et al. 1992a, 1993a, 1993c Hassoun et al. 1993). DNA damage was attributed to oxidative injury caused by endrin. 

Given that oxidative injury plays an important role in central nervous system (CNS) degenerative diseases, novel drags that protect cells from cytopathic effects of ROS could conceivably be used to treat some of these devastating illnesses. To screen for possible neuroprotective drags, a variety of standardized test systems have been designed mostly based on the in situ generation of superoxide by xanthine/xanthine oxidase. Superoxide decomposition may be followed photometrically by the reduction of ferricytochrome c, as it was reported by McCord and Fridovich (McCord and Fridovich, 1969). 

Chamulitrat, W., 1998, Nitric oxide inhibited peroxyl and aUcoxyl radical formation with concomitant protection against oxidant injury in intestinal epithehal cells, A r/t. Biochem. Biophys. 355 206-214. 

Hart, C. M., Tolson, J. K., and Block, E. R., 1991, Supplemental fatty adds alter hpid peroxidation and oxidant injury in endothelial ceUs, Am. J. Physiol. 260 L481-488. 

PolyADP-ribosylation has been reported to play a role in traumatic brain injury (TBI), excitotoxic, and oxidative injury. In the mitochondria after TBI, PARPs are activated and poIyADP-ribosylate multiple proteins involved in electron transfer. Since the ribosylation of these proteins shuts down electron transport, cells are sent into an apoptotic state. This gives insight into mitochondrial-based brain injuries and diseases. 

Bystrum et al. first described morphologic changes in leaf surface waxes of table beet exposed to photochemical oxidants these changes were different from those associated with aphid feeding. Comparison of oxidant injury with that produced by insects has since received attention from Hibben, who found that ozone injury to the leaves of four tree species produced smaller flecks, randomly spaced and darker than fleck injury along veins induced by a mesophyll-feeding leafhopper. 

It is widely believed that vegetation growing in the humid eastern United States would be severely injured if oxidant concentrations reached the daily peak concentrations (0.20-0.40 ppm) commonly experienced in the less humid sections of California. An air pollution episode that occurred on July 27-30, 1970, in the Washington, D.C., area is indicative of what may happen. During this 4-day period, the peak oxidant concentrations ranged from 0.14 to 0.22 ppm and were accompanied by a low concentration of sulfur dioxide (0.04 ppm). Oxidant injury was observed on 31 tree, 15 shrub, and 18 herbaceous species in an area of 72 mi (about 187 km ). Increased emisskm of the precursors of photochemical-oxidant formation could result in repeated episodes of acute injury or even chronic injury to eastern vegetation. 

In perennial v etation, adequate soil moisture in the early season interacts to allow open stomata, and thus oxidant injury occurs. When soil moisture becomes limiting, the nonfunctional stomata of injured leaves may remain open, thus increasing transpiration. The moisture stress induced in the late season is additive with oxidant injury, because both increase defoliation. 

Heagle and Heck found that Bel W, tobacco was predisposed to later oxidant injury by exposure to ambient pollutants. MacdowalP reported the same when the pre-exposure was to low oxidant and the later exposure was also low. Antagonism was noted when both doses were high. 

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