PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15490108-0 2004 Hyperglycaemia-induced superoxide production decreases eNOS expression via AP-1 activation in aortic endothelial cells. Superoxides 23-33 nitric oxide synthase 3 Homo sapiens 55-59 15218542-5 2004 Among many enzymatic systems that are capable of producing O(2)(*-), NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O(2)(*-) in the endothelial cells. Superoxides 59-63 nitric oxide synthase 3 Homo sapiens 124-128 15218542-5 2004 Among many enzymatic systems that are capable of producing O(2)(*-), NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O(2)(*-) in the endothelial cells. Superoxides 165-169 nitric oxide synthase 3 Homo sapiens 124-128 15218542-6 2004 It seems that O(2)(*-) generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O(2)(*-). Superoxides 14-18 nitric oxide synthase 3 Homo sapiens 64-68 15218542-6 2004 It seems that O(2)(*-) generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O(2)(*-). Superoxides 137-141 nitric oxide synthase 3 Homo sapiens 64-68 15777017-2 2004 Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 137-170 12757846-4 2003 In the present study, we show that superoxide generated in several enzymatic or chemical systems (e.g., xanthine/xanthine oxidase, endothelial nitric oxide synthase, or potassium superoxide) oxidizes HE to a fluorescent product (excitation, 480 nm; emission, 567 nm) that is totally different from E+. Superoxides 35-45 nitric oxide synthase 3 Homo sapiens 131-164 12824263-7 2003 RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS). Superoxides 113-123 nitric oxide synthase 3 Homo sapiens 203-236 12824263-7 2003 RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS). Superoxides 113-123 nitric oxide synthase 3 Homo sapiens 238-242 15981946-4 2003 PKC-mediated superoxide production may inactivate nitric oxide (NO) derived from endothelial NOS III, but also may inhibit the activity and/or expression of the NO downstream target, the soluble guanylyl cyclase. Superoxides 13-23 nitric oxide synthase 3 Homo sapiens 93-100 12521608-2 2003 Increased expression of endothelial nitric oxide synthase (eNOS) has been shown to play an important role in maintaining high levels of (*)NO generation to offset the increase in O(2)(*-) that occurs during proliferation. Superoxides 179-183 nitric oxide synthase 3 Homo sapiens 24-57 12657742-11 2003 These data show that TRI alters hsp90 interactions with eNOS and induces eNOS to shift from NO to O2- generation. Superoxides 98-100 nitric oxide synthase 3 Homo sapiens 73-77 12665482-2 2003 When uncoupled from essential cofactors, endothelial nitric oxide synthase (eNOS) produces O2*-. Superoxides 91-95 nitric oxide synthase 3 Homo sapiens 41-74 12665482-2 2003 When uncoupled from essential cofactors, endothelial nitric oxide synthase (eNOS) produces O2*-. Superoxides 91-95 nitric oxide synthase 3 Homo sapiens 76-80 12665482-5 2003 When eNOS is functioning normally, incorporation of Nomega-Nitro-L-Arginine methyl ester (L-NAME, 1 mmol/L), results in increased O2*- detection, as inhibition of NO production prevents NO scavenging of O2*-. Superoxides 130-132 nitric oxide synthase 3 Homo sapiens 5-9 12665482-7 2003 In the remaining 9 CCF patients, incorporation of L-NAME reduced O2*- production by 39%, indicating O2*- production by eNOS uncoupling. Superoxides 100-104 nitric oxide synthase 3 Homo sapiens 119-123 11579094-4 2001 Previously, we showed that DOX undergoes a reductive activation at the reductase domain of endothelial nitric-oxide synthase (eNOS) forming the semiquinone and superoxide (Vasquez-Vivar, J., Martasek, P., Hogg, N., Masters, B. S. S., Pritchard, K. A., Jr., and Kalyanaraman, B. Superoxides 160-170 nitric oxide synthase 3 Homo sapiens 91-124 12489993-1 2002 Previously, we have demonstrated that increased superoxide generation plays a role in the nitric oxide (NO)-mediated inhibition of endothelial NO synthase (NOS III) in endothelial cells (ECs). Superoxides 48-58 nitric oxide synthase 3 Homo sapiens 156-163 12489993-2 2002 In this study we demonstrate that the source of the superoxide is likely due to both NADPH oxidase and NOS III itself. Superoxides 52-62 nitric oxide synthase 3 Homo sapiens 103-110 12489993-8 2002 In conclusion, our results indicate that superoxide and peroxynitrite are involved in the inhibition of NOS III by NO, and that the scavenging of superoxide may be necessary to prevent NOS III inhibition during treatments that involve inhaled NO or NO donors. Superoxides 41-51 nitric oxide synthase 3 Homo sapiens 104-111 11879202-0 2002 The ratio between tetrahydrobiopterin and oxidized tetrahydrobiopterin analogues controls superoxide release from endothelial nitric oxide synthase: an EPR spin trapping study. Superoxides 90-100 nitric oxide synthase 3 Homo sapiens 114-147 11879202-2 2002 Purified endothelial nitric oxide synthase (eNOS) generates superoxide under limited availability of 5,6,7,8-tetrahydrobiopterin (BH(4)). Superoxides 60-70 nitric oxide synthase 3 Homo sapiens 9-42 11879202-2 2002 Purified endothelial nitric oxide synthase (eNOS) generates superoxide under limited availability of 5,6,7,8-tetrahydrobiopterin (BH(4)). Superoxides 60-70 nitric oxide synthase 3 Homo sapiens 44-48 11879202-3 2002 Thus alterations in endothelial BH(4) levels have been postulated to stimulate superoxide production from eNOS. Superoxides 79-89 nitric oxide synthase 3 Homo sapiens 106-110 11879202-4 2002 This possibility was examined by determining the concentration-dependent effects of BH(4), and its analogues, on superoxide formation by eNOS. Superoxides 113-123 nitric oxide synthase 3 Homo sapiens 137-141 11879202-5 2002 Superoxide was quantified by EPR spin trapping, which is the only available technique to quantify superoxide from eNOS. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 114-118 11879202-5 2002 Superoxide was quantified by EPR spin trapping, which is the only available technique to quantify superoxide from eNOS. Superoxides 98-108 nitric oxide synthase 3 Homo sapiens 114-118 11879202-6 2002 Using 5-ethoxycarbonyl-5-methyl-pyrroline N-oxide, we show that only fully reduced BH(4) diminished superoxide release from eNOS, with efficiency BH(4)>6-methyl-BH(4)>5-methyl-BH(4). Superoxides 100-110 nitric oxide synthase 3 Homo sapiens 124-128 11879202-14 2002 Collectively, these results indicate that the ratio between oxidized and reduced BH(4) metabolites tightly regulates superoxide formation from eNOS. Superoxides 117-127 nitric oxide synthase 3 Homo sapiens 143-147 10747895-2 2000 Purified endothelial nitric-oxide synthase (eNOS) can generate superoxide (O(2)) under special conditions but is only known to participate in cell signaling through NO. Superoxides 63-73 nitric oxide synthase 3 Homo sapiens 9-42 11443053-0 2001 Signaling by eNOS through a superoxide-dependent p42/44 mitogen-activated protein kinase pathway. Superoxides 28-38 nitric oxide synthase 3 Homo sapiens 13-17 11443053-1 2001 Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism. Superoxides 201-211 nitric oxide synthase 3 Homo sapiens 14-47 11443053-1 2001 Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism. Superoxides 201-211 nitric oxide synthase 3 Homo sapiens 49-53 11443053-1 2001 Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism. Superoxides 213-217 nitric oxide synthase 3 Homo sapiens 14-47 11443053-1 2001 Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism. Superoxides 213-217 nitric oxide synthase 3 Homo sapiens 49-53 11443053-2 2001 Because mitogen-activated protein kinases (MAPK) have been shown to participate in both reactive oxygen species signaling and TNF-alpha regulation, their possible role in eNOS-derived O(2)(-) signal transduction was examined. Superoxides 184-188 nitric oxide synthase 3 Homo sapiens 171-175 11443053-7 2001 Expression of Gln(361)eNOS, a mutant that produces O(2)(-) but not NO, still resulted in p42/44 MAPK phosphorylation. Superoxides 51-55 nitric oxide synthase 3 Homo sapiens 22-26 10997917-11 2000 Folates, superoxide ions, and peroxynitrite scavengers restore the NO-generating activity to eNOS, collectively suggesting that cellular redox state plays an important role in HCy-suppressed NO-generating function of this enzyme. Superoxides 9-19 nitric oxide synthase 3 Homo sapiens 93-97 11053225-0 2000 Endothelial nitric oxide synthase is a site of superoxide synthesis in endothelial cells treated with glyceryl trinitrate. Superoxides 47-57 nitric oxide synthase 3 Homo sapiens 0-33 10747895-2 2000 Purified endothelial nitric-oxide synthase (eNOS) can generate superoxide (O(2)) under special conditions but is only known to participate in cell signaling through NO. Superoxides 63-73 nitric oxide synthase 3 Homo sapiens 44-48 10747895-2 2000 Purified endothelial nitric-oxide synthase (eNOS) can generate superoxide (O(2)) under special conditions but is only known to participate in cell signaling through NO. Superoxides 75-79 nitric oxide synthase 3 Homo sapiens 9-42 10747895-2 2000 Purified endothelial nitric-oxide synthase (eNOS) can generate superoxide (O(2)) under special conditions but is only known to participate in cell signaling through NO. Superoxides 75-79 nitric oxide synthase 3 Homo sapiens 44-48 10747895-3 2000 Here we show that eNOS regulates tumor necrosis factor alpha (TNFalpha) through a mechanism dependent on the production of O(2) and completely independent of NO. Superoxides 123-127 nitric oxide synthase 3 Homo sapiens 18-22 10747895-7 2000 Similar to the effect of eNOS, a O(2) donor dose-dependently increased TNFalpha production in differentiated U937 cells. Superoxides 33-37 nitric oxide synthase 3 Homo sapiens 25-29 10747895-8 2000 In contrast, cotransfection of superoxide dismutase with eNOS prevented TNFalpha up-regulation, as did partial deletion of the eNOS NADPH binding site, a mutation associated with loss of O(2) production. Superoxides 187-191 nitric oxide synthase 3 Homo sapiens 57-61 10747895-8 2000 In contrast, cotransfection of superoxide dismutase with eNOS prevented TNFalpha up-regulation, as did partial deletion of the eNOS NADPH binding site, a mutation associated with loss of O(2) production. Superoxides 187-191 nitric oxide synthase 3 Homo sapiens 127-131 10747895-9 2000 Thus, eNOS may straddle a bifurcating pathway that can lead to the formation of either NO or O(2), interrelated but often opposing free radical messengers. Superoxides 93-97 nitric oxide synthase 3 Homo sapiens 6-10 9612300-9 1998 A reaction between NO and superoxide would produce peroxynitrite, which could then react with the eNOS protein, resulting in enzyme inactivation. Superoxides 26-36 nitric oxide synthase 3 Homo sapiens 98-102 9689061-0 1998 Superoxide generation by endothelial nitric oxide synthase: the influence of cofactors. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 25-58 9689061-1 1998 The mechanism of superoxide generation by endothelial nitric oxide synthase (eNOS) was investigated by the electron spin resonance spin-trapping technique using 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide. Superoxides 17-27 nitric oxide synthase 3 Homo sapiens 42-75 9689061-1 1998 The mechanism of superoxide generation by endothelial nitric oxide synthase (eNOS) was investigated by the electron spin resonance spin-trapping technique using 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide. Superoxides 17-27 nitric oxide synthase 3 Homo sapiens 77-81 9689061-2 1998 In the absence of calcium/calmodulin, eNOS produces low amounts of superoxide. Superoxides 67-77 nitric oxide synthase 3 Homo sapiens 38-42 9689061-3 1998 Upon activating eNOS electron transfer reactions by calcium/calmodulin binding, superoxide formation is increased. Superoxides 80-90 nitric oxide synthase 3 Homo sapiens 16-20 9689061-7 1998 However, the concomitant addition of L-arginine and tetrahydrobiopterin (BH4) abolishes superoxide generation by eNOS. Superoxides 88-98 nitric oxide synthase 3 Homo sapiens 113-117 9689061-12 1998 Our data indicate that modulation of BH4 concentration may regulate the ratio of superoxide to nitric oxide generated by eNOS. Superoxides 81-91 nitric oxide synthase 3 Homo sapiens 121-125 9333325-0 1997 Endothelial nitric oxide synthase-dependent superoxide generation from adriamycin. Superoxides 44-54 nitric oxide synthase 3 Homo sapiens 0-33 9333325-7 1997 Adriamycin binds to eNOS with a Km of approximately 5 microM, as calculated from both eNOS-dependent NADPH consumption and superoxide generation. Superoxides 123-133 nitric oxide synthase 3 Homo sapiens 20-24 9333325-10 1997 A consequence of eNOS-mediated reductive activation of adriamycin is the disruption of the balance between nitric oxide and superoxide. Superoxides 124-134 nitric oxide synthase 3 Homo sapiens 17-21 9268712-0 1997 Tetrahydrobiopterin regulates superoxide and nitric oxide generation by recombinant endothelial nitric oxide synthase. Superoxides 30-40 nitric oxide synthase 3 Homo sapiens 84-117 9268712-2 1997 Recent in vivo studies suggest that NOS III may also be a source of superoxide production, which would limit its role as a NO-producing enzyme. Superoxides 68-78 nitric oxide synthase 3 Homo sapiens 36-43 9268712-3 1997 In the current study we examined both the NO and the superoxide generating potential of recombinant NOS III obtained from a baculovirus/Sf9 expression system. Superoxides 53-63 nitric oxide synthase 3 Homo sapiens 100-107 9268712-4 1997 Using lucigenin chemiluminesence we could indeed demonstrate (superoxide dismutase inhibitable) superoxide production by NOS III. Superoxides 62-72 nitric oxide synthase 3 Homo sapiens 121-128 9268712-7 1997 Superoxide generation by NOS III could be completely inhibited by diphenyleneiodonium (DPI), an inhibitor of the flavin moiety of the enzyme, indicating that this group is a main source of superoxide production by the enzyme. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 25-32 9268712-7 1997 Superoxide generation by NOS III could be completely inhibited by diphenyleneiodonium (DPI), an inhibitor of the flavin moiety of the enzyme, indicating that this group is a main source of superoxide production by the enzyme. Superoxides 189-199 nitric oxide synthase 3 Homo sapiens 25-32 9268712-10 1997 NOS III thus appears to be a superoxide generating enzyme probably through its flavin moiety, as well as a BH4-dependent NO producing enzyme. Superoxides 29-39 nitric oxide synthase 3 Homo sapiens 0-7 34517018-8 2021 High levels of the phosphorylated monomeric superoxide anion-generating endothelial nitric oxide synthase (eNOS), decreased nitric oxide (NO) bioavailability, decreased soluble guanylyl cyclase (sGC) activity, and high levels of 3-nitrotyrosine were observed in HCM. Superoxides 44-60 nitric oxide synthase 3 Homo sapiens 72-105 8687488-2 1996 In the present study, we demonstrated that NO synthase (cNOS) and xanthine oxidase (XO) of human keratinocytes can be activated to release NO, superoxide (O2-) and peroxynitrite (ONOO-) following exposure to ultraviolet B (UVB) radiation. Superoxides 143-153 nitric oxide synthase 3 Homo sapiens 56-60 8687488-2 1996 In the present study, we demonstrated that NO synthase (cNOS) and xanthine oxidase (XO) of human keratinocytes can be activated to release NO, superoxide (O2-) and peroxynitrite (ONOO-) following exposure to ultraviolet B (UVB) radiation. Superoxides 155-158 nitric oxide synthase 3 Homo sapiens 56-60 8687488-9 1996 ONOO- synthesized by NO and O2- following UVB radiation of cNOS and XO was inhibited by oxypurinol (100 microM). Superoxides 28-30 nitric oxide synthase 3 Homo sapiens 59-63 24578389-12 2015 Reactive oxygen species excess, via NAD(P)H oxidase activation, induces the endothelial nitric oxide synthase uncoupling, which in turn generates superoxide and impairs NO production. Superoxides 146-156 nitric oxide synthase 3 Homo sapiens 76-109 9236411-11 1997 However, upregulation of eNOS and NO release is associated with a marked concomitant increase of O2- production. Superoxides 97-99 nitric oxide synthase 3 Homo sapiens 25-29 34517018-8 2021 High levels of the phosphorylated monomeric superoxide anion-generating endothelial nitric oxide synthase (eNOS), decreased nitric oxide (NO) bioavailability, decreased soluble guanylyl cyclase (sGC) activity, and high levels of 3-nitrotyrosine were observed in HCM. Superoxides 44-60 nitric oxide synthase 3 Homo sapiens 107-111 34356605-7 2021 What is particularly important is the fact that hypoxia contributes to the depletion of cofactor BH4 and deficiency of substrate L-Arg, and thus elicits eNOS uncoupling-a state in which the enzyme produces superoxide instead of NO. Superoxides 206-216 nitric oxide synthase 3 Homo sapiens 153-157 34638028-3 2021 Herein we focus on two enzymes that are key to the biosynthesis of superoxide and nitric oxide, NADPH oxidase 5 (NOX5) and endothelial nitric oxide synthase (eNOS), respectively. Superoxides 67-77 nitric oxide synthase 3 Homo sapiens 123-156 34638028-3 2021 Herein we focus on two enzymes that are key to the biosynthesis of superoxide and nitric oxide, NADPH oxidase 5 (NOX5) and endothelial nitric oxide synthase (eNOS), respectively. Superoxides 67-77 nitric oxide synthase 3 Homo sapiens 158-162 34502464-3 2021 Dysfunctional endothelial nitric oxide synthase (eNOS) produces superoxide anion (O2- ) and contributes to the establishment of a pro-oxidant environment in melanoma. Superoxides 64-80 nitric oxide synthase 3 Homo sapiens 14-47 34502464-3 2021 Dysfunctional endothelial nitric oxide synthase (eNOS) produces superoxide anion (O2- ) and contributes to the establishment of a pro-oxidant environment in melanoma. Superoxides 64-80 nitric oxide synthase 3 Homo sapiens 49-53 34016263-8 2021 Exogenous C16:0-ceramide directly increased superoxide via tetrahydrobiopterin-mediated endothelial nitric oxide synthase uncoupling and dysregulated protein phosphatase 2 in human aortic endothelial cells. Superoxides 44-54 nitric oxide synthase 3 Homo sapiens 88-121 35199130-8 2022 The uncoupled eNOS does not produce NO but produces superoxide. Superoxides 52-62 nitric oxide synthase 3 Homo sapiens 14-18 32351667-7 2020 Converted to a superoxide-producing enzyme, uncoupled eNOS not only leads to reduction of the nitric oxide (NO) generation but also potentiates the preexisting oxidative stress, which contributes significantly to atherogenesis. Superoxides 15-25 nitric oxide synthase 3 Homo sapiens 54-58 32363908-4 2021 CRITICAL ISSUES: Under conditions of tetrahydrobiopterin (BH4) depletion, eNOS generated superoxide trigger pathological events. Superoxides 89-99 nitric oxide synthase 3 Homo sapiens 74-78 26660451-4 2017 Thus, the consequences of the interaction (redox crosstalk) of superoxide/hydrogen peroxide produced by mitochondria with other ROS producing enzymes such as NADPH oxidases (Nox) are of outstanding importance and will be discussed including the consequences for endothelial nitric oxide synthase (eNOS) uncoupling as well as the redox regulation of the vascular function/tone in general (soluble guanylyl cyclase, endothelin-1, prostanoid synthesis). Superoxides 63-73 nitric oxide synthase 3 Homo sapiens 262-295 30738311-2 2019 Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -). Superoxides 212-228 nitric oxide synthase 3 Homo sapiens 68-101 30738311-2 2019 Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -). Superoxides 212-228 nitric oxide synthase 3 Homo sapiens 103-107 30738311-2 2019 Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -). Superoxides 212-228 nitric oxide synthase 3 Homo sapiens 121-125 30738311-2 2019 Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -). Superoxides 230-232 nitric oxide synthase 3 Homo sapiens 68-101 30738311-2 2019 Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -). Superoxides 230-232 nitric oxide synthase 3 Homo sapiens 103-107 30738311-2 2019 Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -). Superoxides 230-232 nitric oxide synthase 3 Homo sapiens 121-125 27184745-4 2016 Endothelial dysfunction is linked to eNOS uncoupling, which consists of a switch from the generation of NO to the generation of superoxide anions and hydrogen peroxide. Superoxides 128-145 nitric oxide synthase 3 Homo sapiens 37-41 25020117-6 2014 Expression of a phosphomimetic T495D eNOS (human isoform) resulted in increased superoxide and diminished nitric oxide (NO) production. Superoxides 80-90 nitric oxide synthase 3 Homo sapiens 37-41 25809076-4 2016 As eNOS produces nitric oxide (NO) and NAD(P)Hoxidase produces superoxide anions (O2 (-) , quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodilator capacity. Superoxides 63-80 nitric oxide synthase 3 Homo sapiens 125-129 25809076-4 2016 As eNOS produces nitric oxide (NO) and NAD(P)Hoxidase produces superoxide anions (O2 (-) , quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodilator capacity. Superoxides 82-84 nitric oxide synthase 3 Homo sapiens 3-7 25809076-4 2016 As eNOS produces nitric oxide (NO) and NAD(P)Hoxidase produces superoxide anions (O2 (-) , quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodilator capacity. Superoxides 82-84 nitric oxide synthase 3 Homo sapiens 125-129 26560496-0 2015 Serine 1179 Phosphorylation of Endothelial Nitric Oxide Synthase Increases Superoxide Generation and Alters Cofactor Regulation. Superoxides 75-85 nitric oxide synthase 3 Homo sapiens 31-64 23836447-9 2015 These results suggest that upregulation of eNOS phosphorylation at Ser1177 and eNOS phosphorylation at Thr495 produce NO and superoxide anions, respectively, resulting in generation of peroxynitrite, which causes impairment of vascular endothelial cells. Superoxides 125-142 nitric oxide synthase 3 Homo sapiens 43-47 23836447-9 2015 These results suggest that upregulation of eNOS phosphorylation at Ser1177 and eNOS phosphorylation at Thr495 produce NO and superoxide anions, respectively, resulting in generation of peroxynitrite, which causes impairment of vascular endothelial cells. Superoxides 125-142 nitric oxide synthase 3 Homo sapiens 79-83 25020117-10 2014 Both hsp90 and caveolin-1 have been shown to influence eNOS uncoupling and a peptide mimicking the scaffolding domain of caveolin-1 blocked the ability of PKCalpha to stimulate eNOS-derived superoxide. Superoxides 190-200 nitric oxide synthase 3 Homo sapiens 177-181 25020117-11 2014 Collectively, these results suggest that the G+ pore-forming toxins promote increased EC permeability via activation of PKCalpha, phosphorylation of eNOS-T495, loss of hsp90 and caveolin-1 binding which collectively promote eNOS uncoupling and the production of barrier disruptive superoxide. Superoxides 281-291 nitric oxide synthase 3 Homo sapiens 224-228 25460725-3 2014 Production of RMs mainly superoxide (O2(-)) has been found in a variety of predominating cellular enzyme systems including NAD(P)H oxidase, xanthine oxidase (XO), cyclooxygenase (COX), uncoupled endothelial nitric oxide synthase (eNOS) and myeloperoxidase (MPO). Superoxides 25-35 nitric oxide synthase 3 Homo sapiens 195-228 24863258-1 2014 (6R)-5,6,7,8-Tetrahydro-L-biopterin (BH4) availability regulates nitric oxide and superoxide formation by endothelial nitric oxide synthase (eNOS). Superoxides 82-92 nitric oxide synthase 3 Homo sapiens 106-139 24405159-9 2014 Transfection studies with wild-type and mutant human eNOS confirmed the dual role of eNOS as a producer of superoxide anion (O2-) with SIN-1 treatment, and a producer of NO in the presence of DMPO. Superoxides 107-123 nitric oxide synthase 3 Homo sapiens 53-57 24405159-9 2014 Transfection studies with wild-type and mutant human eNOS confirmed the dual role of eNOS as a producer of superoxide anion (O2-) with SIN-1 treatment, and a producer of NO in the presence of DMPO. Superoxides 107-123 nitric oxide synthase 3 Homo sapiens 85-89 24405159-9 2014 Transfection studies with wild-type and mutant human eNOS confirmed the dual role of eNOS as a producer of superoxide anion (O2-) with SIN-1 treatment, and a producer of NO in the presence of DMPO. Superoxides 125-128 nitric oxide synthase 3 Homo sapiens 53-57 24405159-9 2014 Transfection studies with wild-type and mutant human eNOS confirmed the dual role of eNOS as a producer of superoxide anion (O2-) with SIN-1 treatment, and a producer of NO in the presence of DMPO. Superoxides 125-128 nitric oxide synthase 3 Homo sapiens 85-89 24959009-3 2014 Production of RMs mainly superoxides ( O2 (-)) has been found in a variety of predominating cellular enzyme systems including nicotinamide adenine dinucleotide phosphate oxidase, xanthine oxidase, cyclooxygenase, endothelial nitric oxide synthase (eNOS) and myeloperoxidase. Superoxides 25-36 nitric oxide synthase 3 Homo sapiens 213-246 24959009-3 2014 Production of RMs mainly superoxides ( O2 (-)) has been found in a variety of predominating cellular enzyme systems including nicotinamide adenine dinucleotide phosphate oxidase, xanthine oxidase, cyclooxygenase, endothelial nitric oxide synthase (eNOS) and myeloperoxidase. Superoxides 39-41 nitric oxide synthase 3 Homo sapiens 213-246 25460725-3 2014 Production of RMs mainly superoxide (O2(-)) has been found in a variety of predominating cellular enzyme systems including NAD(P)H oxidase, xanthine oxidase (XO), cyclooxygenase (COX), uncoupled endothelial nitric oxide synthase (eNOS) and myeloperoxidase (MPO). Superoxides 37-39 nitric oxide synthase 3 Homo sapiens 195-228 23965989-2 2013 Bioavailability of BH4 is a critical factor in regulating the balance between NO and superoxide production by endothelial NOS (eNOS coupling). Superoxides 85-95 nitric oxide synthase 3 Homo sapiens 127-131 23965989-7 2013 eNOS-derived superoxide production was significantly elevated in W447A and W447F versus wild-type eNOS, and this was sufficient to oxidize BH4 to 7,8-dihydrobiopterin. Superoxides 13-23 nitric oxide synthase 3 Homo sapiens 0-4 23965989-7 2013 eNOS-derived superoxide production was significantly elevated in W447A and W447F versus wild-type eNOS, and this was sufficient to oxidize BH4 to 7,8-dihydrobiopterin. Superoxides 13-23 nitric oxide synthase 3 Homo sapiens 98-102 23965989-11 2013 These data reveal a key role for Trp-447 in determining NO versus superoxide production by eNOS, by effects on BH4-dependent catalysis, and by modulating eNOS dimer formation. Superoxides 66-76 nitric oxide synthase 3 Homo sapiens 91-95 20540939-10 2010 Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions. Superoxides 225-242 nitric oxide synthase 3 Homo sapiens 118-133 23395155-5 2013 In BH4 deficiency, oxygen reduction uncouples from NO synthesis, thereby converting eNOS to a superoxide-producing enzyme. Superoxides 94-104 nitric oxide synthase 3 Homo sapiens 84-88 22333037-9 2012 Endothelial nitric oxide synthase may produce both superoxide anion (( )O(2)(-)) and nitric oxide (NO) leading to peroxynitrite (( )ONOO(-)) generation. Superoxides 51-67 nitric oxide synthase 3 Homo sapiens 0-33 21797845-1 2012 BACKGROUND AND PURPOSE: One key mechanism for endothelial dysfunction is endothelial NOS (eNOS) uncoupling, whereby eNOS generates superoxide (O(2) ( -) ) rather than NO. Superoxides 131-141 nitric oxide synthase 3 Homo sapiens 73-88 21797845-1 2012 BACKGROUND AND PURPOSE: One key mechanism for endothelial dysfunction is endothelial NOS (eNOS) uncoupling, whereby eNOS generates superoxide (O(2) ( -) ) rather than NO. Superoxides 143-147 nitric oxide synthase 3 Homo sapiens 73-88 21724868-0 2011 Suppression of eNOS-derived superoxide by caveolin-1: a biopterin-dependent mechanism. Superoxides 28-38 nitric oxide synthase 3 Homo sapiens 15-19 21724868-2 2011 In the absence of the requisite eNOS cofactor tetrahydrobiopterin (BH(4)), NADPH oxidation is uncoupled from NO generation, leading to the production of superoxide. Superoxides 153-163 nitric oxide synthase 3 Homo sapiens 32-36 21724868-4 2011 In the current study, we investigated the effects of both BH(4) depletion and oxidation on eNOS-derived superoxide production in endothelial cells in an attempt to elucidate the molecular mechanisms regulating eNOS oxidase activity. Superoxides 104-114 nitric oxide synthase 3 Homo sapiens 91-95 21724868-9 2011 Moreover, when caveolin-1 silencing was combined with a pharmacological inhibitor of AKT, BH(4) depletion increased eNOS-derived superoxide to 165% of that observed with BH(4) oxidation. Superoxides 129-139 nitric oxide synthase 3 Homo sapiens 116-120 21198553-8 2011 NADPH-oxidase-derived superoxide avidly reacts with eNOS-derived NO to form peroxynitrite (ONOO(-)). Superoxides 22-32 nitric oxide synthase 3 Homo sapiens 52-56 23549379-5 2013 Using a prechiasmatic injection model of SAH, we show here that eNOS knockout (KO) significantly alleviates vasospasm of the middle cerebral artery and reduces superoxide production. Superoxides 160-170 nitric oxide synthase 3 Homo sapiens 64-68 23781221-3 2013 Increasing number of studies from recent years demonstrates that uncoupling of endothelial nitric oxide synthase (eNOS), whereby the enzyme eNOS produces detrimental amount of superoxide anion [Formula: see text] instead the vasoprotective nitric oxide (NO( )), plays a critical role in vascular dysfunction under various pathophysiological conditions and in aging. Superoxides 176-192 nitric oxide synthase 3 Homo sapiens 79-112 22996620-7 2013 Moreover, a small amount of O2- induced by water extracts from fermented soy milk at low concentration (1 mg mL-1) increased the content of calcium ions and activated eNOS, thereby promoting NO production and the coupling state of eNOS. Superoxides 28-30 nitric oxide synthase 3 Homo sapiens 167-171 22996620-7 2013 Moreover, a small amount of O2- induced by water extracts from fermented soy milk at low concentration (1 mg mL-1) increased the content of calcium ions and activated eNOS, thereby promoting NO production and the coupling state of eNOS. Superoxides 28-30 nitric oxide synthase 3 Homo sapiens 231-235 22609206-3 2012 The endothelial nitric oxide synthase (eNOS)-inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) reduced superoxide formation in platelets identifying "uncoupled" eNOS as a superoxide source. Superoxides 107-117 nitric oxide synthase 3 Homo sapiens 4-37 22609206-3 2012 The endothelial nitric oxide synthase (eNOS)-inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) reduced superoxide formation in platelets identifying "uncoupled" eNOS as a superoxide source. Superoxides 175-185 nitric oxide synthase 3 Homo sapiens 4-37 22167522-3 2012 Uncoupling of eNOS, with subsequently less NO and more superoxide generation, is one of the major underlying causes of endothelial dysfunction found in atherosclerosis, diabetes, hypertension, cigarette smoking, hyperhomocysteinemia, and ischemia/reperfusion injury. Superoxides 55-65 nitric oxide synthase 3 Homo sapiens 14-18 21642378-4 2011 Furthermore, new data are presented that provide novel insights into how disruption of the eNOS dimer prevents eNOS uncoupling and the production of superoxide under conditions of elevated oxidative stress and identifies a novel regulatory region we have termed the "flexible arm". Superoxides 149-159 nitric oxide synthase 3 Homo sapiens 91-95 21642378-4 2011 Furthermore, new data are presented that provide novel insights into how disruption of the eNOS dimer prevents eNOS uncoupling and the production of superoxide under conditions of elevated oxidative stress and identifies a novel regulatory region we have termed the "flexible arm". Superoxides 149-159 nitric oxide synthase 3 Homo sapiens 111-115 21666221-0 2011 Superoxide induces endothelial nitric-oxide synthase protein thiyl radical formation, a novel mechanism regulating eNOS function and coupling. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 19-52 21666221-0 2011 Superoxide induces endothelial nitric-oxide synthase protein thiyl radical formation, a novel mechanism regulating eNOS function and coupling. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 115-119 21666221-3 2011 We demonstrate endothelial NOS (eNOS) oxidant-induced protein thiyl radical formation from tetrahydrobiopterin-free enzyme or following exposure to exogenous superoxide using immunoblotting, immunostaining, and mass spectrometry. Superoxides 158-168 nitric oxide synthase 3 Homo sapiens 15-30 21666221-3 2011 We demonstrate endothelial NOS (eNOS) oxidant-induced protein thiyl radical formation from tetrahydrobiopterin-free enzyme or following exposure to exogenous superoxide using immunoblotting, immunostaining, and mass spectrometry. Superoxides 158-168 nitric oxide synthase 3 Homo sapiens 32-36 21666221-4 2011 Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme. Superoxides 191-201 nitric oxide synthase 3 Homo sapiens 144-148 21666221-4 2011 Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme. Superoxides 191-201 nitric oxide synthase 3 Homo sapiens 308-312 21666221-9 2011 Furthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNOS protein radical formation, as visualized with confocal microscopy, was increased, and these results were confirmed by immunoprecipitation with anti-eNOS antibody, followed by immunoblotting with an anti-DMPO antibody. Superoxides 77-87 nitric oxide synthase 3 Homo sapiens 100-104 21666221-9 2011 Furthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNOS protein radical formation, as visualized with confocal microscopy, was increased, and these results were confirmed by immunoprecipitation with anti-eNOS antibody, followed by immunoblotting with an anti-DMPO antibody. Superoxides 77-87 nitric oxide synthase 3 Homo sapiens 253-257 21666221-10 2011 Thus, eNOS protein radical formation provides the basis for a mechanism of superoxide-directed regulation of eNOS, involving thiol oxidation, defining a unique pathway for the redox regulation of cardiovascular function. Superoxides 75-85 nitric oxide synthase 3 Homo sapiens 6-10 21666221-10 2011 Thus, eNOS protein radical formation provides the basis for a mechanism of superoxide-directed regulation of eNOS, involving thiol oxidation, defining a unique pathway for the redox regulation of cardiovascular function. Superoxides 75-85 nitric oxide synthase 3 Homo sapiens 109-113 21261471-1 2011 Oxidative stress has been shown to convert endothelial nitric oxide synthase (eNOS) from an NO-producing enzyme to an enzyme that generates superoxide, a process termed NOS uncoupling. Superoxides 140-150 nitric oxide synthase 3 Homo sapiens 43-76 21147698-9 2010 The reduced affinity of eNOS to the cofactor BH4 may lead to insufficient NO, but increased superoxide production in preeclamptic placentas. Superoxides 92-102 nitric oxide synthase 3 Homo sapiens 24-28 21179168-1 2010 Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)( -)), which are key mediators of cellular signalling. Superoxides 137-147 nitric oxide synthase 3 Homo sapiens 0-33 21179168-1 2010 Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)( -)), which are key mediators of cellular signalling. Superoxides 137-147 nitric oxide synthase 3 Homo sapiens 35-39 20540939-10 2010 Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions. Superoxides 225-242 nitric oxide synthase 3 Homo sapiens 135-139 20540939-12 2010 Data suggest that balloon catheter injury promoted eNOS uncoupling in contralateral carotids, which generates superoxide rather than NO, and reduces phenylephrine-induced extracellular calcium mobilization, despite the hyper-reactivity to phenylephrine in contralateral carotids. Superoxides 110-120 nitric oxide synthase 3 Homo sapiens 51-55 21188246-2 2010 Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury. Superoxides 181-191 nitric oxide synthase 3 Homo sapiens 81-85 19946124-0 2010 Beta-actin association with endothelial nitric-oxide synthase modulates nitric oxide and superoxide generation from the enzyme. Superoxides 89-99 nitric oxide synthase 3 Homo sapiens 28-61 19946124-7 2010 Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells. Superoxides 222-232 nitric oxide synthase 3 Homo sapiens 57-61 19946124-7 2010 Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells. Superoxides 222-232 nitric oxide synthase 3 Homo sapiens 119-123 19946124-7 2010 Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells. Superoxides 222-232 nitric oxide synthase 3 Homo sapiens 119-123 19946124-8 2010 Disruption of eNOS-beta-actin interaction in endothelial cells using ABS peptide 326 resulted in decreased NO production, increased superoxide formation, and decreased endothelial monolayer wound repair, which was prevented by PEG-SOD and NO donor NOC-18. Superoxides 132-142 nitric oxide synthase 3 Homo sapiens 14-18 19946124-9 2010 Taken together, this novel finding indicates that beta-actin binding to eNOS through residues 326-333 in the eNOS protein results in shifting the enzymatic activity from superoxide formation toward NO production. Superoxides 170-180 nitric oxide synthase 3 Homo sapiens 72-76 19946124-9 2010 Taken together, this novel finding indicates that beta-actin binding to eNOS through residues 326-333 in the eNOS protein results in shifting the enzymatic activity from superoxide formation toward NO production. Superoxides 170-180 nitric oxide synthase 3 Homo sapiens 109-113 19946124-10 2010 Modulation of NO and superoxide formation from eNOS by beta-actin plays an important role in endothelial function. Superoxides 21-31 nitric oxide synthase 3 Homo sapiens 47-51 19398669-8 2009 Both MTHFR genotype and vascular 5-MTHF were associated with vascular nitric oxide bioavailability and superoxide generated by uncoupled endothelial nitric oxide synthase. Superoxides 103-113 nitric oxide synthase 3 Homo sapiens 137-170 21063103-0 2010 Opposite effect of Hsp90alpha and Hsp90beta on eNOS ability to produce nitric oxide or superoxide anion in human embryonic kidney cells. Superoxides 87-103 nitric oxide synthase 3 Homo sapiens 47-51 18716321-0 2008 Targeted increases in endothelial cell superoxide anion production stimulate eNOS-dependent nitric oxide production, not uncoupled eNOS activity. Superoxides 39-55 nitric oxide synthase 3 Homo sapiens 77-81 19176602-4 2009 Activity of NOS3 was characterized by conversion of arginine to citrulline, BH(4) intracellular availability, cGMP, and superoxide anion production. Superoxides 120-136 nitric oxide synthase 3 Homo sapiens 12-16 19176602-7 2009 In aged cells with an uncoupled NOS3 as shown by the reduced BH(4) level, the increase in superoxide anion and the lower production of cGMP and the decrease in NO bioavailability were linearly correlated with the increase in basal [Ca(2+)](i). Superoxides 90-106 nitric oxide synthase 3 Homo sapiens 32-36 19011239-2 2009 In the absence of BH4, eNOS becomes "uncoupled" and generates superoxide rather than NO. Superoxides 62-72 nitric oxide synthase 3 Homo sapiens 23-27 19011239-7 2009 Intracellular BH4 deficiency induced superoxide generation from eNOS, as assessed by N-nitro-L-arginine methyl ester inhibitable 2-hydroxyethidium generation, and attenuated NO production. Superoxides 37-47 nitric oxide synthase 3 Homo sapiens 64-68 19011239-9 2009 Furthermore, increasing the intracellular BH2 concentration in the presence of a constant eNOS:BH4 ratio was sufficient to induce eNOS-dependent superoxide production. Superoxides 145-155 nitric oxide synthase 3 Homo sapiens 90-94 19011239-9 2009 Furthermore, increasing the intracellular BH2 concentration in the presence of a constant eNOS:BH4 ratio was sufficient to induce eNOS-dependent superoxide production. Superoxides 145-155 nitric oxide synthase 3 Homo sapiens 130-134 18622039-0 2008 Phosphorylation of endothelial nitric-oxide synthase regulates superoxide generation from the enzyme. Superoxides 63-73 nitric oxide synthase 3 Homo sapiens 19-52 18382884-4 2008 Superoxide produced by the NADPH oxidase may react with NO released by the endothelial nitric oxide synthase (eNOS) thereby generating peroxynitrite (ONOO-), leading to eNOS uncoupling and therefore eNOS-mediated superoxide production. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 75-108 18398337-10 2008 CYBA C242T and NOS3 G894T polymorphisms had additive effects on vascular superoxide generation (P = 0.026) and xanthine oxidase activity was increased in patients with CAD (P = 0.043). Superoxides 73-83 nitric oxide synthase 3 Homo sapiens 15-19 18382884-4 2008 Superoxide produced by the NADPH oxidase may react with NO released by the endothelial nitric oxide synthase (eNOS) thereby generating peroxynitrite (ONOO-), leading to eNOS uncoupling and therefore eNOS-mediated superoxide production. Superoxides 213-223 nitric oxide synthase 3 Homo sapiens 75-108 17486142-6 2007 Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation. Superoxides 234-244 nitric oxide synthase 3 Homo sapiens 14-18 17413035-3 2007 When endothelial nitric oxide synthase is 6R-BH4-deplete, it synthesizes superoxide rather than nitric oxide. Superoxides 73-83 nitric oxide synthase 3 Homo sapiens 5-38 17486142-6 2007 Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation. Superoxides 234-244 nitric oxide synthase 3 Homo sapiens 87-91 17327434-1 2007 Uncoupling of the endothelial nitric oxide synthase (eNOS) resulting in superoxide anion (O(2)(-)) formation instead of nitric oxide (NO) causes diabetic endothelial dysfunction. Superoxides 72-88 nitric oxide synthase 3 Homo sapiens 18-51 17327434-1 2007 Uncoupling of the endothelial nitric oxide synthase (eNOS) resulting in superoxide anion (O(2)(-)) formation instead of nitric oxide (NO) causes diabetic endothelial dysfunction. Superoxides 90-95 nitric oxide synthase 3 Homo sapiens 18-51 16585403-8 2006 Diminished levels of BH4 promote O2*- production by eNOS (referred to as eNOS uncoupling). Superoxides 33-35 nitric oxide synthase 3 Homo sapiens 52-56 17293058-4 2007 Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 97-101 17293058-4 2007 Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 158-162 17293058-4 2007 Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator. Superoxides 193-203 nitric oxide synthase 3 Homo sapiens 97-101 16585403-8 2006 Diminished levels of BH4 promote O2*- production by eNOS (referred to as eNOS uncoupling). Superoxides 33-35 nitric oxide synthase 3 Homo sapiens 73-77 16226933-6 2005 Nicotinamide adenine dinucleotide phosphate oxidase and the uncoupled endothelial nitric oxide synthase may be O2- -producing enzymes. Superoxides 111-113 nitric oxide synthase 3 Homo sapiens 70-103 16528409-3 2006 FFA-induced overproduction of superoxide activated a variety of proinflammatory signals previously implicated in hyperglycemia-induced vascular damage and inactivated 2 important antiatherogenic enzymes, prostacyclin synthase and eNOS. Superoxides 30-40 nitric oxide synthase 3 Homo sapiens 230-234 16293798-1 2006 This article explores the physiology of superoxide generation by endothelial nitric oxide synthase (eNOS), the so-called "uncoupled" state of the enzyme. Superoxides 40-50 nitric oxide synthase 3 Homo sapiens 65-98 16293798-1 2006 This article explores the physiology of superoxide generation by endothelial nitric oxide synthase (eNOS), the so-called "uncoupled" state of the enzyme. Superoxides 40-50 nitric oxide synthase 3 Homo sapiens 100-104 16009356-2 2005 Enzymatic systems such as the mitochondrial respiratory chain, vascular NAD(P)H oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS) produce superoxide anion (O2*-) in vascular cells. Superoxides 171-187 nitric oxide synthase 3 Homo sapiens 122-155 16009356-2 2005 Enzymatic systems such as the mitochondrial respiratory chain, vascular NAD(P)H oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS) produce superoxide anion (O2*-) in vascular cells. Superoxides 189-191 nitric oxide synthase 3 Homo sapiens 122-155 16195486-4 2005 This is caused by increased vascular superoxide production and a supersensitivity to vasoconstrictors secondary to a tonic activation of protein kinase C. NADPH oxidase(s) and uncoupled endothelial nitric oxide synthase have been proposed as superoxide sources. Superoxides 37-47 nitric oxide synthase 3 Homo sapiens 186-219 16195486-4 2005 This is caused by increased vascular superoxide production and a supersensitivity to vasoconstrictors secondary to a tonic activation of protein kinase C. NADPH oxidase(s) and uncoupled endothelial nitric oxide synthase have been proposed as superoxide sources. Superoxides 242-252 nitric oxide synthase 3 Homo sapiens 186-219 15879305-3 2005 Superoxide produced by the NADPH oxidase may react with NO released by endothelial nitric oxide synthase (eNOS), thereby generating peroxynitrite. Superoxides 0-10 nitric oxide synthase 3 Homo sapiens 71-104 15721870-9 2005 In COS-7 cells, a T495A eNOS mutant generated significantly more O(2)(-) than a T495D mutant did, indicating that the dephosphorylation of Thr(495) alone can increase O(2)(-) production by eNOS. Superoxides 167-171 nitric oxide synthase 3 Homo sapiens 24-28 15941833-1 2005 Recent studies demonstrate that oxidative inactivation of tetrahydrobiopterin (H4B) may cause uncoupling of endothelial nitric oxide synthase (eNOS) to produce superoxide (O2*-). Superoxides 160-170 nitric oxide synthase 3 Homo sapiens 108-141 15941833-1 2005 Recent studies demonstrate that oxidative inactivation of tetrahydrobiopterin (H4B) may cause uncoupling of endothelial nitric oxide synthase (eNOS) to produce superoxide (O2*-). Superoxides 172-174 nitric oxide synthase 3 Homo sapiens 108-141 15925745-4 2005 When uncoupled from essential cofactors, NO synthase III (NOS III) can also produce O(2)(*-). Superoxides 84-88 nitric oxide synthase 3 Homo sapiens 41-56 15925745-4 2005 When uncoupled from essential cofactors, NO synthase III (NOS III) can also produce O(2)(*-). Superoxides 84-88 nitric oxide synthase 3 Homo sapiens 58-65 15925745-10 2005 A reduction in O(2)(*-) production in response to L-NAME occurred in the remaining patients and indicates O(2)(*-) production by the uncoupled NOS III enzyme. Superoxides 15-19 nitric oxide synthase 3 Homo sapiens 143-150 15925745-10 2005 A reduction in O(2)(*-) production in response to L-NAME occurred in the remaining patients and indicates O(2)(*-) production by the uncoupled NOS III enzyme. Superoxides 15-23 nitric oxide synthase 3 Homo sapiens 143-150 15925745-11 2005 CONCLUSIONS: This study provides first published evidence that NOS III can reside in the uncoupled state in patients with hypertension and, to a greater extent, in patients with coexisting hypertension and diabetes, and that it contributes significantly to increased superoxide production in these disease states. Superoxides 267-277 nitric oxide synthase 3 Homo sapiens 63-70 15721870-1 2005 OBJECTIVE: Oxidized low-density lipoprotein (ox-LDL) increases superoxide anion (O(2)(-)) production by the endothelial nitric oxide (NO) synthase (eNOS). Superoxides 63-79 nitric oxide synthase 3 Homo sapiens 148-152 15721870-1 2005 OBJECTIVE: Oxidized low-density lipoprotein (ox-LDL) increases superoxide anion (O(2)(-)) production by the endothelial nitric oxide (NO) synthase (eNOS). Superoxides 81-84 nitric oxide synthase 3 Homo sapiens 148-152 15721870-9 2005 In COS-7 cells, a T495A eNOS mutant generated significantly more O(2)(-) than a T495D mutant did, indicating that the dephosphorylation of Thr(495) alone can increase O(2)(-) production by eNOS. Superoxides 65-69 nitric oxide synthase 3 Homo sapiens 24-28