Nitrosative stress

Bile Adds Induce Oxidative/Nitrosative Stress in Cells of the GI Tract... 

Table 3.3 Bile acids induce oxidative/nitrosative stress in cells of the GI tract. ...

Klatt P, Lamas S. 2000. Regulation of protein function by S-glutathiolation in response to oxidative and nitrosative stress. Fur J Biochem 267 4928 4944. 

Volume 440. Nitric Oxide, Part F Oxidative and Nitrosative Stress in Redox... 

Hyperglycemia, Oxidative/Nitrosative Stress, and G-protein/Adenylyl Cyclase Signaling... 

Pacher, P., I.G. Obrosova, J.G. Mabley, and C. Szabo. 2005. Role of nitrosative stress and peroxynitrite in the pathogenesis of diabetic complications. Emerging new therapeutical strategies. Curr. Med. Chem. 12 267-275. 

Nitrosative stress occurs when the generation of RNS in a system exceeds the system s ability to eliminate them. Since ROS and RNS are generally highly reactive, they react with key organic substances such as lipids, proteins, and DNA [5]. Oxidation of these biomolecules can damage them and may be responsible to a variety of diseases. 

In general, oxidative and nitrosative stress result from an imbalance between an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) on one side and a deficiency of enzymatic and... 

Sommer D, Coleman S, Swanson SA, Stemmer PM. 2002. Differential susceptibilities of serine/threonine phosphatases to oxidative and nitrosative stress. Arch Biochem Biophys... 

Moreover, targeted disruption (knock-down) of the eNOS gene attenuates the neuronal cell death in thiamine-deficient mice (Gibson and Zhang, 2002). eNOS knock-down but not knock-down of iNOS or nNOS leads to a reduction in protein tyrosine nitration (Beauchesne et al., 2009), suggesting a major role of eNOS as the source of nitric oxide-related nitrosative stress in thiamine deficiency. 

Another marker for protein oxidation is nitration of tyrosine residues, and numerous previous studies support the notion that nitrosative stress also contributes to neurodegeneration in AD (Smith et al., 1997 Tohgi et al., 1999 Castegna et al, 2003 Sultana et al., 2006b). A number of mechanisms for tyrosine nitration of protein have been proposed, and the two widely believed to exist in vivo involve formation of peroxynitrite or mediation via hemeperoxidases (Brennan et al., 2002). These mechanisms involve NO or its by-products that react with ROS (Beckman et al. 

Kato, K., Mizoi, M., An, Y., Nakano, M., Wanibuchi, H., Endo, G., Endo, Y., Hoshino, M., Okada, S., Yamanaka, K. (2007). Oral administration of diphenylarsinic acid, a degradation product of chemical warfare agents, induces oxidative and nitrosative stress in cerebellar Purkinje cells. Life Sci. 81 1518-25. 

Szabo G, Bahrle S. Role of nitrosative stress and poly(ADP-ribose) polymerase activation in myocardial reperfusion injury. Curr. Vase. Pharmacol. 2005 3 215-220. 

NADH peroxidase (Npx EC 1.11.1.1) and NADH oxidase (Nox EC 1.6.99.x) are disulfide oxidoreductases-related enzymes that contain a single redox-active cysteine (16). They supply strictly fermentative bacteria with NAD+ for glycolysis and play an important role in redox signaling in response to oxidative and nitrosative stress (19). 

Chronic hyperglycemia induces numerous alterations in the vasculature that accelerate the atherosclerotic process. Several major mechanisms contribute to the pathological alterations in blood vessels in diabetes, including 1) the nonenzymatic glyco-sylation of proteins and lipids, which form advanced glycation endproducts (AGEs) that can interfere with their normal function and 2) the induction of oxidative and nitrosative stress, as well as exacerbation of proinflammatory responses (50). These abnormalities lead to impaired endogenous platelet inhibition and platelet activation, which could result in arterial thrombosis, and consequently myocardial infarction and stroke (51). 

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