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Nitric oxide oxidant stress

NO Nitric oxide/oxidative stress, inflamation, irradiation Oxidation of cysteines in DNA-binding domain Calmels et al. (1997)... [Pg.89]

McLeod, T.M., Lopez-Figueroa, A.L., and Lopez-Figueroa, M.O. 2001. Nitric oxide, stress, and depression. Psychopharmacol. Bull. 35 24-41. [Pg.366]

Kudo FA, Warycha B, Juran PJ, Asada H, Teso D, Aziz F (2005) Differential responsiveness of early- and late-passage endothehal cells to shear stress. Am J Surg 190(5) 763-769 Lee RH, Efron D, Tantry U, Barbul A (2001) Nitric oxide in the healing wound a time-course study. J Surg Res 101(1) 104-108... [Pg.349]

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. [Pg.210]

D.L. Kellogg, J.L. Zhao, C. Friel and LJ. Roman, Nitric oxide concentration increases in the cutaneous interstitial space during heat stress in humans. J. Appl. Physiol. 94, 1971-1977 (2003). [Pg.52]

In conclusion, it should be stressed that the competition between pro- and antiapoptotic effects of nitric oxide must probably depends on its relevant levels [137] the low physiological levels of NO principally suppress the apoptotic pathway by several mechanisms, whereas the higher rates of NO production may overcome cellar protective mechanisms and stimulate apoptosis. Furthermore, the simultaneous formation of nitric oxide and superoxide increases the possibility of apoptosis activation due to the formation of peroxynitrite. [Pg.759]

Belkner et al. [32] demonstrated that 15-LOX oxidized preferably LDL cholesterol esters. Even in the presence of free linoleic acid, cholesteryl linoleate continued to be a major LOX substrate. It was also found that the depletion of LDL from a-tocopherol has not prevented the LDL oxidation. This is of a special interest in connection with the role of a-tocopherol in LDL oxidation. As the majority of cholesteryl esters is normally buried in the core of a lipoprotein particle and cannot be directly oxidized by LOX, it has been suggested that LDL oxidation might be initiated by a-tocopheryl radical formed during the oxidation of a-tocopherol [33,34]. Correspondingly, it was concluded that the oxidation of LDL by soybean and recombinant human 15-LOXs may occur by two pathways (a) LDL-free fatty acids are oxidized enzymatically with the formation of a-tocopheryl radical, and (b) the a-tocopheryl-mediated oxidation of cholesteryl esters occurs via a nonenzymatic way. Pro and con proofs related to the prooxidant role of a-tocopherol were considered in Chapter 25 in connection with the study of nonenzymatic lipid oxidation and in Chapter 29 dedicated to antioxidants. It should be stressed that comparison of the possible effects of a-tocopherol and nitric oxide on LDL oxidation does not support importance of a-tocopherol prooxidant activity. It should be mentioned that the above data describing the activity of cholesteryl esters in LDL oxidation are in contradiction with some earlier results. Thus in 1988, Sparrow et al. [35] suggested that the 15-LOX-catalyzed oxidation of LDL is accelerated in the presence of phospholipase A2, i.e., the hydrolysis of cholesterol esters is an important step in LDL oxidation. [Pg.810]

Wassmann S, Laufs U, Stamenkovic D, Linz W, Stasch JP, Ahlbory K, Rosen R, Bohm M, Nickening G (2002) Raloxifene improves endothelial dysfunction in hypertension by reduced oxidative stress and enhanced nitric oxide production. Circulation 105 2083-2091... [Pg.90]

Intramuscular injection of turpentine causes a biphasic HPA response [33], The first phase corresponds to the stress of injection with no detectable changes in plasma IL-6 concentrations. However, the second phase coincides with an inflammatory response to the turpentine, a response accompanied by increased plasma ACTH, corticosterone, and IL-6 levels. CRH, AVP, and PGs play stimulatory roles in this model, whereas nitric oxide dampens the pituitary response [33], IL-ip may be important for triggering the release of these signaling molecules, since mice lacking the gene for IL-ip have a blunted GC response to turpentine [34],... [Pg.496]

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... [Pg.233]

Vardi A, Formiggini F, Casotti R, De Martino A, Ribalet F, Miralto A, Bowler C (2006) A stress surveillance system based on calcium and nitric oxide in marine diatoms. PLoS Biol 4 411 119 Vorwerk S, Somerville S, Somerville C (2004) The role of plant cell wall polysaccharide composition in disease resistance. Trends Plant Sci 9 203-209 Vreeland V, Laetsch WM (1990) A gelling carbohydrate in algal cell wall formation. In Adair WS, Mecham RP (eds) Organization and assembly of plant and animal extracellular matrix. Academic, San Diego, CA, ppl 37—171... [Pg.270]

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). [Pg.4]

Fabisiak, J.P., Tyuiin, V.A., Tyurina, Y.Y., Sedlov, A., Lazo, J.S., and Kagan, V.E., 2000, Nitric oxide dissociates lipid oxidation from apoptosis and phosphatidylserine externalization during oxidative stress. Biochemistry 39 127-138. [Pg.92]

Sergent, O., Griffon, B., Morel, I., Chevanne, M., Dubos, M. P., Cihard, P., and Chlard, J., 1997, Effect of nitric oxide on iron-mediated oxidative stress in primary rat hepatocyte culture, Hepatology 25 122-127. [Pg.120]

Huwiler, A., Pfeilschifter, J., and Van den Bosch, H., 1999, Nitric oxide donors induce stress signaling via ceramide formation in rat renal mesangial cells. J. Biol. Chem. 21 A. 7190-7195. [Pg.202]

Figure 19.17 The biochemistiy and physiology responsible for penile erection. Sexual activity itself begins with a state of arousal that leads to erection. Arousal results in part from stimulation of the sense organs. The hypothalamus coordinates the sensations and activates the autonomic nervous system. Sensory nerves from the skin of the penis and other erogenous zones stimulate the parasympathetic system. This activates nitric oxide synthase and the resultant nitric oxide, via cyclic GMP, causes vasodilation of the arterioles. This increases blood flow through the corpora cavernosa which then expands producing an erection. Pheromones secreted by the female can stimulate the odour detecting system in the nasal cavity of the male (Chapter 12 and see above). Stress, however, activates the sympathetic system releases cyclic AMP which can result in vasoconstriction of the arterioles. Other factors that can interfere with an erection are physical fatigue and alcohol. Figure 19.17 The biochemistiy and physiology responsible for penile erection. Sexual activity itself begins with a state of arousal that leads to erection. Arousal results in part from stimulation of the sense organs. The hypothalamus coordinates the sensations and activates the autonomic nervous system. Sensory nerves from the skin of the penis and other erogenous zones stimulate the parasympathetic system. This activates nitric oxide synthase and the resultant nitric oxide, via cyclic GMP, causes vasodilation of the arterioles. This increases blood flow through the corpora cavernosa which then expands producing an erection. Pheromones secreted by the female can stimulate the odour detecting system in the nasal cavity of the male (Chapter 12 and see above). Stress, however, activates the sympathetic system releases cyclic AMP which can result in vasoconstriction of the arterioles. Other factors that can interfere with an erection are physical fatigue and alcohol.
Fe(CN)5(NO)] makes several appearances in a recent symposium volume dedicated to nitric oxide in biosystems, for example in cormection with iron(II) dtrate-induced oxidative stress." " Nitroprusside is the only metal nitrosyl complex in clinical use, where it is important as a rapidly acting agent for the lowering of exceptionally high blood pressure. ... [Pg.430]


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See also in sourсe #XX -- [ Pg.19 ]




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