Disease relevance of NSC334318

• Therefore, to explore the role of oxidized HDL in the pathogenesis of vascular disease, we used MS to quantify 3-chlorotyrosine in HDL isolated from plasma and atherosclerotic tissue [1].
• The detection of 3-chlorotyrosine in HDL isolated from vascular lesions raises the possibility that MPO, by virtue of its ability to form HOCl, may promote atherogenesis by counteracting the established antiatherogenic effects of HDL and the ATP-binding cassette transporter A1 pathway [1].
• Mass spectrometric analysis revealed that levels of 3-chlorotyrosine in E. coli proteins increased markedly after the bacteria were internalized by human neutrophils [2].
• In this investigation, we treated Staphylococcus aureus with varying concentrations of reagent hypochlorous acid and found that even at sublethal doses, it converted some tyrosine residues in their proteins to 3-chlorotyrosine and 3,5-dichlorotyrosine [3].
• We also measured levels of 3-chlorotyrosine as an index of neutrophil activation to assess indirectly the effects of inhaled.NO on lung inflammation [4].

Psychiatry related information on NSC334318

• 3-Chlorotyrosine, a bio-marker of hypochlorous acid (HOCl) in vivo, was reported to be substantially elevated in the Alzheimer's disease (AD) brains [5].

High impact information on NSC334318

• Both models developed an intense neutrophil inflammatory response, and the inflammatory fluid contained markedly elevated levels of 3-chlorotyrosine, a marker of myeloperoxidase action [6].
• These results indicate that 3-chlorotyrosine is a specific marker for LDL oxidation by myeloperoxidase [7].
• The detection of 3-chlorotyrosine in human atherosclerotic lesions indicates that halogenation reactions catalyzed by the myeloperoxidase system of phagocytes constitute one pathway for protein oxidation in vivo [7].
• Moreover, activation of human neutrophils adherent to a L-tyrosine coated glass surface also stimulated 3-chlorotyrosine formation [8].
• In vitro studies demonstrated that chlorination of the aromatic ring of free L-tyrosine was mediated by Cl2 and not by HOCl/ClO-. Thus, 3-chlorotyrosine serves as a specific marker for Cl2-dependent oxidation of free L-tyrosine [8].

Chemical compound and disease context of NSC334318

• Plasma protein levels of 3-nitrotyrosine and 3-chlorotyrosine were measured by LC-MS/MS at 0 and 72 h after the initiation of inhaled nitric oxide (INO) at 20 ppm in 22 prematurely born infants with clinically documented bronchopulmonary dysplasia [9].

Biological context of NSC334318

• To explore the role of activated phagocytes in oxidative stress in chronic renal failure, we used 3-chlorotyrosine as a specific marker of myeloperoxidase activity [10].
• 3-Chlorotyrosine levels (at 1 wk after birth) correlated negatively with birth weight or gestational age [11].

Anatomical context of NSC334318

• Levels of 3-chlorotyrosine were elevated in HDL isolated from the blood of humans with established coronary artery disease, suggesting that circulating levels of oxidized HDL represent a unique marker for clinically significant atherosclerosis [1].
• We also examined intradialytic 3-chlorotyrosine levels using membranes that activate white blood cells and the alternative pathway of complement [10].
• Neutrophil counts in CF sputum correlated strongly with the presence of 3-chlorotyrosine (r2=0.869) [12].
• Recent MS studies indicate that HDL isolated from patients with cardiovascular disease contains elevated levels of 3-chlorotyrosine and 3-nitrotyrosine, which are two characteristic products of myeloperoxidase (MPO), a heme enzyme secreted by macrophages [13].

Associations of NSC334318 with other chemical compounds

• High density lipoprotein (HDL) isolated from human atherosclerotic lesions and the blood of patients with established coronary artery disease contains elevated levels of 3-nitrotyrosine and 3-chlorotyrosine [14].
• Following in vitro stimulation, purified peripheral blood neutrophils generated 3-chlorotyrosine, while eosinophils produced predominantly 3-bromotyrosine and 3,5-dibromotyrosine [12].

Gene context of NSC334318

• Hemodialysis increased plasma myeloperoxidase and the expression of CD11b/CD18 by circulating phagocytes, but failed to demonstrably increase 3-chlorotyrosine levels [10].
• Myeloperoxidase and 3-chlorotyrosine levels in BALF from children with CF were 10- and fivefold higher, respectively, than in disease control subjects [15].
• Levels of 3-chlorotyrosine (0.23 vs. 0.14 mmol Cl-Tyr/mol Tyr; medians p = .11) and protein carbonyls (0.347 vs. 0.339 nmol/mg protein; medians p = .56) were not significantly increased in asthmatics [16].

Analytical, diagnostic and therapeutic context of NSC334318

• The assay combines gas chromatography with stable isotope dilution mass spectrometry, and it detects attomole levels of 3-chlorotyrosine in a single determination [17].
• Utilizing isotope dilution gas chromatography-mass spectrometry, we compared 3-chlorotyrosine levels in plasma proteins of five patients on chronic hemodialysis therapy with those of age- and sex-matched healthy controls [10].

References