18-Oxygen Inhalation Method for Determination of Total Body Formation of Nitric Oxide in Humans

Sakinis, Augustinas; Jungersten, Lennart; Nathorst-Westfelt, U.; Stenqvist, O.; Wennmalm, Åke

doi:10.1016/s0021-5198(19)41491-1

Cited by 2 publications

(4 citation statements)

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“…Lipids (for liposomes) were from Avanti Polar Lipids (Birmingham, AL). 18 O 2 was from Larodan Fine Chemical (Malmö, Sweden) and was mixed with 16 O 2 prior to use (25).…”

Section: Methodsmentioning

confidence: 99%

“…Incorporation of 18 O 2 into oxysterols was performed essentially as described (25). Briefly, a healthy male volunteer was exposed for 30 min to room air enriched with a mixture of 16 O 2 and 18 O 2 (in a ratio of about 3:1), in a closed breathing circuit.…”

Section: Exposure To 18 O 2 -Enriched Airmentioning

confidence: 99%

“…The 18 O 2 technique was used to study the in vivo synthesis and oxidation of NO (25). An identical approach was used to study the formation of oxysterols in a healthy volunteer.…”

Section: Use Of 18 O 2 -And 2 H-labeled Cholesterol As Tools For Studies Of Cholesterol Metabolism In Humansmentioning

confidence: 99%

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Evidence that the major oxysterols in human circulation originate from distinct pools of cholesterol: a stable isotope study

Meaney

Hassan

Sakinis

et al. 2001

Journal of Lipid Research

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The major oxysterols in human circulation are 7 ␣ -, 27-, and (24 S )-hydroxycholesterol. Two unique experiments were performed to elucidate their origin and kinetics. A volunteer was exposed to 18 O 2 -enriched air. A rapid incorporation of 18 O in both 7 ␣ -and 27-hydroxycholesterol and disappearance of label after exposure were observed. The half-life was estimated to be less than 1 h. Incorporation of 18 O in (24 S )-hydroxycholesterol was not significant. In the second experiment a volunteer was infused with liposomes containing 10 g of [ 2 H 6 ]cholesterol. This resulted in an enrichment of plasma cholesterol with 2 H of up to 13%, and less than 0.5% in cerebrospinal fluid cholesterol. The content of 2 H in circulating 7 ␣ -hydroxycholesterol remained approximately equal to that of plasma cholesterol and decreased with a half-life of about 13 days. The 2 H content of circulating 27-hydroxycholesterol was initially lower than that of cholesterol but in the last phase of the experiment it exceeded that of cholesterol. No significant incorporation of 2 H in (24 S )-hydroxycholesterol was observed. It is evident that 7 ␣ -hydroxycholesterol must originate from a rapidly miscible pool, about 80% of 27-hydroxycholesterol from a more slowly exchangeable pool, and more than 90% of (24 S )-hydroxycholesterol from a nonexchangeable pool, presumably the brain. The results are discussed in relation to the role of oxysterols in cholesterol homeostasis and their use as markers for pathological conditions. -Meaney,

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“…Lipids (for liposomes) were from Avanti Polar Lipids (Birmingham, AL). 18 O 2 was from Larodan Fine Chemical (Malmö, Sweden) and was mixed with 16 O 2 prior to use (25).…”

Section: Methodsmentioning

confidence: 99%

Section: Exposure To 18 O 2 -Enriched Airmentioning

confidence: 99%

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Evidence that the major oxysterols in human circulation originate from distinct pools of cholesterol: a stable isotope study

Meaney

Hassan

Sakinis

et al. 2001

Journal of Lipid Research

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“…Under pathophysiological conditions, the rate of NO • production was linked with the etiopathogenesis of the disease, with increased immune and inflammatory responses triggering greater rates of NO • production. In the case of animal models, the physiological production of NO • in rats and humans was comparable (0.55 ± 0.05 versus 0.38 ± 0.06 μmol kg –1 h –1 ) but considerably lower than that of mice (7.68 ± 1.47 μmol kg –1 h –1 ). − Therefore, human infectious and inflammatory diseases may not be accurately reproduced by mouse models.…”

Section: Biological Sources and Levels Of No•mentioning

confidence: 99%

Connecting the Chemical and Biological Properties of Nitric Oxide

Toledo

Augusto

2012

Chem. Res. Toxicol.

237

210

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Nitric oxide (NO•; nitrogen monoxide) is known to be a critical regulator of cell and tissue function through mechanisms that utilize its unique physicochemical properties as a small and uncharged free radical with limited reactivity. Here, the basic chemistry and biochemistry of NO• are summarized through the description of its chemical reactivity, biological sources, physiological and pathophysiological levels, and cellular transport. The complexity of the interactions of NO• with biotargets, which vary from irreversible second-order reactions to reversible formation of nonreactive and reactive nitrosyl complexes, is noted. Emphasis is placed on the kinetics and physiological consequences of the reactions of NO• with its better characterized biotargets. These targets are soluble guanylate cyclase (sCG), oxyhemoglobin/hemoglobin (HbO2/Hb) and cytochrome c oxidase (CcOx), all of which are ferrous heme proteins that react with NO• with second-order rate constants approaching the diffusion limit (k on approximately 107 to 108 M–1 s–1). Likewise, the biotarget responsible for the most described pathophysiological actions of NO• is the superoxide anion radical (O2 •–), which reacts with NO• in a diffusion-controlled process (k approximately 1010 M–1 s–1). The reactions of NO• with proteins containing iron–sulfur clusters ([FeS]) remain little studied and the reported rate constants of the first steps of these reactions are considerable (k approximately 105 M–1 s–1). Not surprisingly, the interactions of proteins containing iron–sulfur clusters with NO• remain ambiguous and have been associated with both physiological and pathophysiological effects. Overall, it is emphasized that any claimed biological action of NO• should be connected with its interaction with kinetically relevant biotargets. Although reactivity toward biotargets is only one of the factors contributing to cellular and tissue responses mediated by short-lived species, such as NO• and other oxygen-derived species, it is a critical factor. Therefore, taking reactivity into account is important to advancing our knowledge on redox signaling mechanisms.

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18-Oxygen Inhalation Method for Determination of Total Body Formation of Nitric Oxide in Humans

Cited by 2 publications

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Evidence that the major oxysterols in human circulation originate from distinct pools of cholesterol: a stable isotope study

Evidence that the major oxysterols in human circulation originate from distinct pools of cholesterol: a stable isotope study

Connecting the Chemical and Biological Properties of Nitric Oxide

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