Reactive Nitrogen Species and Proteins: Biological Significance and Clinical Relevance

Nitration of a Critical Tyrosine Residue in the Allosteric Inhibitor Site of Muscle Glycogen Phosphorylase Impairs its Catalytic Activity

“…5,7,28 We tested whether peroxynitrite-dependent inactivation of GPb could be due to thiol residue modifications by exposing GPb (T or R form) at a final concentration of 1.25 μM to various concentrations of four reagents that modify cysteine residues. These reagents included N-ethylmaleimide, iodoacetamide, H 2 O 2 and Hg 2+ .…”

“…4,5 Peroxynitrite affects protein functions by modifying essential reactive thiol groups 6 and/or tyrosine residues, thereby leading to the formation of oxidized thiol groups or of 3-nitrotyrosine (3NT). 7,8 Peroxynitrite has numerous physiological functions, especially in skeletal muscle cells. These functions include contraction, glucose uptake, metabolism and signaling.…”

“…[4][5][6][7][8] Peroxynitrite is one of the most reactive, and therefore most deleterious, NO derivatives involved in the oxidative modification of biological molecules. 4,5 Peroxynitrite affects protein functions by modifying essential reactive thiol groups 6 and/or tyrosine residues, thereby leading to the formation of oxidized thiol groups or of 3-nitrotyrosine (3NT).…”

An epigrammatic (abridged) recounting of the myriad tales of astonishing deeds and dire consequences pertaining to nitric oxide and reactive oxygen species in mitochondria with an ancillary missive concerning the origins of apoptosis

“…However, when excessive quantities of NO are generated during inflammation or neuronal hyper-stimulation, significant quantities of potentially tissue injuring peroxynitrite may be formed ( Fig. 1; Souza et al, 2001;Dedon and Tannenbaum, 2004;Keynes and Garthwaite, 2004).…”

Dietary vitamin D deficiency in rats from middle to old age leads to elevated tyrosine nitration and proteomics changes in levels of key proteins in brain: Implications for low vitamin D-dependent age-related cognitive decline

“…Prior studies have shown that cognitively impaired subjects have significant levels of mitochondrial dysfunction and oxidative protein damage. In particular, nitration of protein resident tyrosine residues is a common marker observed in brain of cognitively impaired subjects [30–34]. Therefore, we tested the hypothesis that manipulating serum VitD levels would alter protein nitration and key protein markers of mitochondrial function.…”