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- Bakker, Emily, et al.
(författare)
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Acute dietary nitrate supplementation improves arterial endothelial function at high altitude : A double-blinded randomized controlled cross over study
- 2015
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Ingår i: Nitric oxide. - : Elsevier BV. - 1089-8603 .- 1089-8611. ; 50, s. 58-64
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Dietary nitrate (NO3-) supplementation serves as an exogenous source of nitrite (NO3-) and nitric oxide (NO) through the NO3- NO3- NO pathway, and may improve vascular functions during normoxia. The effects of NO3- supplementation in healthy lowlanders during hypobaric hypoxia are unknown. Purpose: Determine the effect of acute oral NO3- supplementation via beetroot juice (BJ) on endothelial function (flow mediated dilation; FMD) in lowlanders at 3700 m. Methods: FMD was measured using ultrasound and Doppler in the brachial artery of 11 healthy subjects (4 females, age 25 +/- 5 yrs; height 1.8 +/- 0.1 m, weight 72 +/- 10 kg) sojourning to high altitude. In a randomized, double-blinded crossover study design, FMD was measured 3 h after drinking BJ (5.0 mmol NO3-) and placebo (PL; 0.003 mmol No-3(-)) supplementation at 3700 m, with a 24-h wash out period between tests. FMD was also measured without any BJ supplementation pre-trek at 1370 m, after 5 days at 4200 m and upon return to 1370 m after 4 weeks of altitude exposure (above 2500 m). The altitude exposure was interrupted by a decent to lower altitude where subjects spent two nights at 1370 m before returning to altitude again. Results: Ten subjects completed the NO3- supplementation. FMD (mean +/- SD) pre-trek value was 6.53 +/- 2.32% at 1370 m. At 3700 m FMD was reduced to 3.84 +/- 1.31% (p < 0.01) after PL supplementation but was normalized after receiving BJ (5.77 +/- 1.14% (p = 1.00). Eight of the subjects completed the interrupted 4-week altitude stay, and their FMD was lower at 4200 m (FMD 3.04 +/- 2.22%) and at post-altitude exposure to 1370 m (FMD 3.91 +/- 2.58%) compared to pre-trek FMD at 1370 m. Conclusion: Acute dietary NO3- supplementation may abolish altitude-induced reduction in endothelial function, and can serve as a dietary strategy to ensure peripheral vascular function in lowland subjects entering high altitude environments. (C) 2015 Elsevier Inc. All rights reserved.
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- Bueno, Emilio, et al.
(författare)
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Disparate response to microoxia and nitrogen oxides of the Bradyrhizobium japonicum napEDABC, nirK and norCBQD denitrification genes
- 2017
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Ingår i: Nitric oxide. - : Elsevier. - 1089-8603 .- 1089-8611. ; 68, s. 137-149
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Tidskriftsartikel (refereegranskat)abstract
- Expression of the Bradyrhizobium japonicum napEDABC, nirK and norCBQD denitrification genes requires low oxygen (O-2) tension and nitrate (NO3), through a regulatory network comprised of two coordinated cascades, FixLJ-FixK(2)-NnrR and RegSR-NifA. To precisely understand how these signals are integrated in the FixLJ-FixK(2)-NnrR circuit, we analyzed beta-Galactosidase activities from napE-lacZ, nirK-lacZ and norC-lacZ fusions, and performed analyses of NapC and NorC levels as well as periplasmic nitrate reductase (Nap) activity, in B. japonicum wildtype and fixK(2) and nnrR mutant backgrounds. While microoxic conditions (2% O-2 at headspace) were sufficient to induce expression of napEDABC and nirK genes and this control depends on FixK(2), norCBQD expression requires, in addition to microoxia, nitric oxide gas (NO) and both FixK(2) and NnrR transcription factors. Purified FixK(2) protein directly interacted and activated transcription in collaboration with B. japonicum RNA polymerase (RNAP) from the napEDABC and nirK promoters, but not from the norCBQD promoter. Further, recombinant NnrR protein bound exclusively to the norCBQD promoter in an O-2-sensitive manner. Our work suggest a disparate regulation of B. japonicum denitrifying genes expression with regard to their dependency to microoxia, nitrogen oxides (NOx), and the regulatory proteins FixK(2) and NnrR. In this control, expression of napEDABC and nirK genes requires microoxic conditions and directly depends on FixK2, while expression of norCBQD genes relies on NO, being NnrR the candidate which directly interacts with the norCBQD promoter.
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- Carlsson, S., et al.
(författare)
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Effects of pH, nitrite, and ascorbic acid on nonenzymatic nitric oxide generation and bacterial growth in urine
- 2001
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Ingår i: Nitric oxide. - : Elsevier BV. - 1089-8603 .- 1089-8611. ; 5:6, s. 580-586
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Nitrite may be generated by bacteria in urine during urinary tract infections. Acidification of nitrite results in the formation of nitric oxide (NO) and other reactive nitrogen oxides, which are toxic to a variety of microorganisms. We have studied NO formation and bacterial growth in mildly acidified human urine containing nitrite and the reducing agent vitamin C. Urine collected from healthy subjects was incubated in closed syringes at different pH values with varying amounts of nitrite and/or ascorbic acid added. NO generation was measured in headspace gas using a chemiluminescence technique. A similar setup was also used to study the growth of three strains of bacteria in urine. Mildly acidified nitrite-containing urine generated large amounts of NO and this production was greatly potentiated by ascorbic acid. The growth of Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus saprophyticus was markedly reduced by the addition of nitrite to acidified urine. This inhibition was enhanced by ascorbic acid. In conclusion, we show that the growth of three common urinary pathogens is markedly inhibited in mildly acidified urine when nitrite is present. The bacteriostatic effect of acidified nitrite is likely related to the release of NO and other toxic reactive nitrogen intermediates. These results may help to explain the well-known beneficial effects of urinary acidification with, e.g., vitamin C in treatment and prevention of urinary tract infection.
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- Carlström, Mattias, et al.
(författare)
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Peritoneal dialysis impairs nitric oxide homeostasis and may predispose infants with low systolic blood pressure to cerebral ischemia
- 2016
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Ingår i: Nitric Oxide - Biology and Chemistry. - : Elsevier BV. - 1089-8603 .- 1089-8611. ; 58, s. 1-9
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Tidskriftsartikel (refereegranskat)abstract
- Background & purpose Infants on chronic peritoneal dialysis (PD) have an increased risk of developing neurological morbidities; however, the underlying biological mechanisms are poorly understood. In this clinical study, we investigated whether PD-mediated impairment of nitric oxide (NO) bioavailability and signaling, in patients with persistently low systolic blood pressure (SBP), can explain the occurrence of cerebral ischemia. Methods & results Repeated blood pressure measurements, serial neuroimaging studies, and investigations of systemic nitrate and nitrite levels, as well as NO signaling, were performed in ten pediatric patients on PD. We consistently observed the loss of both inorganic nitrate (-17 ± 3%, P < 0.05) and nitrite (-34 ± 4%, P < 0.05) during PD, which may result in impairment of the nitrate-nitrite-NO pathway. Indeed, PD was associated with significant reduction of cyclic guanosine monophosphate levels (-59.4 ± 15%, P < 0.05). This reduction in NO signaling was partly prevented by using a commercially available PD solution supplemented with l-arginine. Although PD compromised nitrate-nitrite-NO signaling in all cases, only infants with persistently low SBP developed ischemic cerebral complications. Conclusions Our data suggests that PD impairs NO homeostasis and predisposes infants with persistently low SBP to cerebral ischemia. These findings improve current understanding of the pathogenesis of infantile cerebral ischemia induced by PD and may lead to the new treatment strategies to reduce neurological morbidities.
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