Inhibition of Luminol-Enhanced Chemiluminescence by Reduced Pterins

Shen, Rong‐Sen

doi:10.1006/abbi.1994.1140

Cited by 23 publications

(11 citation statements)

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“…A critical question that must be addressed is whether BH4-induced improvements in endothelial dysfunction in chronic smokers are secondary to its effects on the uncoupled NOS III or whether they simply reflect antioxidant actions described for reduced pteridines. 20 Indeed, by using lucigenin-enhanced chemiluminescence, we found that BH4 as well as NH4 potently scavenged superoxide generated in vitro by the xanthine/xanthine oxidase reaction in a dosedependent fashion (see Figure 6). …”

Section: Discussionmentioning

confidence: 89%

“…20 To test whether BH4-induced improvements on FBF in chronic smokers are due to its specific effects on the uncoupled NOS III or secondary to its antioxidant properties, we tested in an additional group of 15 smokers equimolar concentrations (50 mol/L) of BH4 and NH4 on the ACh dose-response relationship on 2 separate days.…”

Section: Protocol 3: Effects Of Nh4 and Bh4 On Endothelial Dysfunctiomentioning

confidence: 99%

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Tetrahydrobiopterin Improves Endothelium-Dependent Vasodilation in Chronic Smokers

Heitzer

Brockhoff

Mayer

et al. 2000

Circulation Research

410

278

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Abstract-Conditions associated with impaired nitric oxide (NO) activity and accelerated atherosclerosis have been shown to be associated with a reduced bioavailability of tetrahydrobiopterin (BH4). We therefore hypothesized that BH4 supplementation may improve endothelial dysfunction of chronic smokers. Forearm blood flow (FBF) responses to the endothelium-dependent vasodilators acetylcholine (ACh; 0.75, 1.5, and 3.0 g/100 mL tissue/min) or serotonin (5-HT; 0.7, 2.1, and 6.3 ng/100 mL tissue/min), to the inhibitor of endothelial nitric oxide synthase (NOS) N G -monomethyl-L-arginine (L-NMMA; 2, 4, and 8 mol/min), and to the endothelium-independent vasodilator sodium nitroprusside (SNP; 0.1, 0.3, and 1.0 g/100 mL tissue/min) were measured by venous occlusion plethysmography in controls and chronic smokers. Drugs were infused into the brachial artery, and FBF was measured before and during concomitant intra-arterial infusion of BH4, tetrahydroneopterin (NH4; another reduced pteridine), or the antioxidant vitamin C (6 and 18 mg/min). In control subjects, BH4 had no effect on FBF in response to ACh, 5-HT, and SNP. In contrast, in chronic smokers, the attenuated FBF responses to ACh and 5-HT were markedly improved by concomitant administration of BH4, whereas the vasodilator responses to SNP were not affected. L-NMMA-induced vasoconstriction was significantly reduced in smokers compared with controls, suggesting impaired basal NO bioactivity. BH4 improved L-NMMA responses in smokers while having no effect on L-NMMA responses in controls. Pretreatment with vitamin C abolished BH4 effects on ACh-dependent vasodilation. In vitro, NH4 scavenged superoxide created by the xanthine/xanthine oxidase reaction equipotent like BH4 but failed to modify ACh-induced changes in FBF in chronic smokers in vivo. These data support the concept that in addition to the free radical burden of cigarette smoke, a dysfunctional NOS III due to BH4 depletion may contribute at least in part to endothelial dysfunction in chronic smokers. The full text of this article is available at http://www.circresaha.org. (Circ Res. 2000;86:e36-e41.)

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Section: Discussionmentioning

confidence: 89%

Section: Protocol 3: Effects Of Nh4 and Bh4 On Endothelial Dysfunctiomentioning

confidence: 99%

Tetrahydrobiopterin Improves Endothelium-Dependent Vasodilation in Chronic Smokers

Heitzer

Brockhoff

Mayer

et al. 2000

Circulation Research

410

278

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“…Consistently, in the present study, supplementation of bEnd.3 cells with BH4, at least in part, restored eNOS activity in the presence of OA and prevented OA-induced reactive oxygen species production. On the other hand, it is also possible Q4 that the decrease in reactive oxygen species production is caused by the direct antioxidant properties of BH4 (Shen, 1994) independent of its interaction with eNOS. Alternatively, BH4 may act directly on mitochondrial oxygen radical production.…”

Section: Discussionmentioning

confidence: 97%

Oleic acid increases mitochondrial reactive oxygen species production and decreases endothelial nitric oxide synthase activity in cultured endothelial cells

Gremmels

Bevers

Fledderus

et al. 2015

European Journal of Pharmacology

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“…35 However, this is unlikely because BH 4 supplementation enhanced hepatic BH 4 levels without increasing the levels of its oxidized forms. The main mechanisms for the beneficial effects of BH 4 supplementation appear to be an amelioration of eNOS uncoupling.…”

Section: Discussionmentioning

confidence: 99%

The eNOS cofactor tetrahydrobiopterin improves endothelial dysfunction in livers of rats with CCl4 cirrhosis

et al. 2006

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In cirrhosis, intrahepatic endothelial dysfunction is one of the mechanisms involved in the increased resistance to portal blood flow and therefore in the development of portal hypertension. Endothelial nitric oxide synthase (eNOS) uncoupling due to deficiency of tetrahydrobiopterin (BH 4 ) results in decreased production of NO and plays a major role in endothelial dysfunction in other conditions. We examined whether eNOS uncoupling is involved in the pathogenesis of endothelial dysfunction of livers with cirrhosis. Basal levels of tetrahydrobiopterin and guanosine triphosphate (GTP)-cyclohydrolase (BH 4 rate-limiting enzyme) expression and activity were determined in liver homogenates of control and rats with CCl 4 cirrhosis. Thereafter, rats were treated with tetrahydrobiopterin, and eNOS activity, NO bioavailability, assessed with a functional assay, and the vasodilator response to acetylcholine (endothelial function) were evaluated. Livers with cirrhosis showed reduced BH 4 levels and decreased GTPcyclohydrolase activity and expression, which were associated with impaired vasorelaxation to acetylcholine. Tetrahydrobiopterin supplementation increased BH 4 hepatic levels and eNOS activity and significantly improved the vasodilator response to acetylcholine in rats with cirrhosis. In conclusion, the impaired response to acetylcholine of livers with cirrhosis is modulated by a reduced availability of the eNOS cofactor, tetrahydrobiopterin. Tetrahydrobiopterin supplementation improved the endothelial dysfunction of cirrhotic livers. (HEPATOLOGY 2006;44:44-52.)

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Inhibition of Luminol-Enhanced Chemiluminescence by Reduced Pterins

Cited by 23 publications

References 0 publications

Tetrahydrobiopterin Improves Endothelium-Dependent Vasodilation in Chronic Smokers

Tetrahydrobiopterin Improves Endothelium-Dependent Vasodilation in Chronic Smokers

Oleic acid increases mitochondrial reactive oxygen species production and decreases endothelial nitric oxide synthase activity in cultured endothelial cells

The eNOS cofactor tetrahydrobiopterin improves endothelial dysfunction in livers of rats with CCl4 cirrhosis

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