Reactive oxygen species , nitric oxide

Similar to reactive oxygen species, nitric oxide, peroxynitrite, and other nitrogen oxide species produced by mitochondria are able to stimulate or inhibit apoptosis. Proapoptotic effect of nitric oxide was probably first shown by Albina et al. [138], who demonstrated NO-induced... 

In addition to reactive oxygen species, nitric oxide may be a potential mediator of sihca-induced toxicity (Castranova et al. 1996). Nitric oxide adsorbed readily to DQ12 quartz (Robertson et al. 1982). At room temperature it remained adsorbed for up to several weeks. Thermal desorption of NO was much lower (43 %) than of NOj (67 %). Vallya-THAN et al. (1997) studied the kinetic clearance of instilled stable nitroxide radicals (2,2,6,6-tetra-methyl piperidine N-oxyl) and showed an oxidative stress in adult male Sprague-Dawley rats exposed to 10 mg Min-U-Sil quartz <5 im. The generation of reactive oxygen species increased by sihca was associated with enhanced levels of superoxide dismu-tase (P<0.05) and lipid peroxidation. 

Redox reactions involving nitric oxide have important implications beyond their fundamental chemistry as demonstrated by the controversy in the biomedical literature regarding conditions under which generation of NO leads to the amelioration or the exacerbation of oxidative stress in mammalian systems (95). Oxidative stress is defined as a disturbance in the balance between production of reactive oxygen species (pro-oxidants) and antioxidant defenses (96). Reactive oxygen species include free radicals and peroxides as well as other reactants such as oxidative enzymes with metal ion sites in high oxidation states. The... 

Crow JP (1997) DichlorodUiydrofluorescein and dihydrorhodamine 123 are sensitive indicators of peroxynitrite in vitro implications for intracellular measurement of reactive nitrogen and oxygen species. Nitric Oxide 1 145-157... 

Hu, C. et al., Black rice (Oryza sativa L. indica) pigmented fraction suppresses both reactive oxygen species and nitric oxide in chemical and biological model systems, J. Agric. Food Chem., 51, 5271, 2003. 

Results of a more recent series of investigations suggest that lead may cause hypertension in rats by increasing reactive oxygen species, which act as vasoconstrictors, and decreasing nitric oxide, a vasodilator released by the endothelium. The reactive oxygen species may be the hydroxyl radical, and did not appear to be the superoxide anion (Ding et al. 1998). 

The formation of nitric oxide in microsomes results in the inhibition of microsomal reductase activity. It has been found that the inhibitory effect of nitric oxide mainly depend on the interaction with cytochrome P-450. NO reversibly reacts with P-450 isoforms to form the P-450-NO complex, but at the same time it irreversibly inactivates the cytochrome P-450 via the modification of its thiol residues [64]. Incubation of microsomes with nitric oxide causes the inhibition of 20-HETE formation from arachidonic acid [65], the generation of reactive oxygen species [66], and the release of catalytically active iron from ferritin [67],... 

Mitochondria, nitric oxide synthase and arachidonic acid metabolism are sources of reactive oxygen species during ischemia—reperfusion injury 568... 

Nitric oxide and peroxynitrite contribute to oxidative damage 569 Production of eicosanoids from polyunsaturated fatty acids such as arachidonic acid may generate reactive oxygen species 570 Brain antioxidant defenses modify ischemia-reperfusion injury 570 Reactive oxygen species may modify both the excitotoxic and the apoptotic components of ischemic brain damage 570... 

Mitochondria, nitric oxide synthase and arachidonic acid metabolism are sources of reactive oxygen species during ischemia-reperfusion injury. ROS generation during ischemia-reperfusion may come from several sources, including NOS activity, mitochondrial electron transport, multiple steps in the metabolism of arachidonic... 

Gunasekar PG, Sun PW, Kanthasamy AG, etal. 1996. Cyanide-induced neurotoxcity involves nitric oxide and reactive oxygen species generation after N-Methyl-D-aspartate receptor activation. The Journal of Pharmacology and Experimental Therapeutics 277 150-155. 

Antonsson and Marinou 2000 Adams and Cory, 1998). Stress may also cause inaease, nitric oxide (NO), or reactive oxygen species (ROS) production which, in turn, triggers release of apoptotic proteins from the intermemhrane space (Kroemer and Reed, 2000 Vieira et at, 2000). Release of these proteins from mitochondria are required for stress induced killing hut are, with a few exceptions (Bergmann et al, 1994, Schulze- Osthoff et al, 1993), dispensible for CD95 and TNF-receptor transduced apoptosis. These other death processes require FADD and caspase-8 to be recruited into the death receptor complexes and cannot be blocked by Bcl-2 (Krammer, 2000 Scaffidi et al, 1998). 

Wink, D. A., Cook, J. A., Pacelh, R., Liebmann, J., Krishna, M. C., and Mitchell, J. B., 1995, Nitric oxide (NO) protects against ceUular damage by reactive oxygen species, Toxicol. Lett. 82-83 221-226. 

Nitric oxide protects against cellular damage and cytotoxicity from reactive oxygen species, Proc. Natl. Acad. Sci. USA 90 9813-9817. 

Cutaneous reactions such as rash or Stevens-Johnson syndrome are also consist with initiation through protein haptenation, although in this case dendritic cell activation/ migration and T-cell propagation are involved [31]. Other immune mediators such as cytokines, nitric oxide and reactive oxygen species which may be linked to the formation of reactive metabolites may also be implicated, as may specific processes occurring at the level of the keratinocyte. 

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