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Open AccessJournal ArticleDOI

Macrophages can convert citrulline into arginine.

Guoyao Wu, +1 more
- 01 Jan 1992 - 
- Vol. 281, Iss: 1, pp 45-48
TLDR
The results demonstrate that citrulline, produced by NO synthetase, can be recycled to arginine in macrophages, and may contribute to the regulation of intracellular availability of argininine and thus the prolonged production of NO by macrophage.
Abstract
Rat peritoneal macrophages were incubated in the presence of 0.05-1.0 mM-[14C]citrulline. The synthesis of [14C]arginine from 0.1 mM-[14C]citrulline was about 300 pmol/h per 10(6) cells in macrophages from saline-injected (control) rats. Both arginine synthesis from citrulline and nitrate production (an indicator of NO generation) were increased about 3-fold in the cells from lipopolysaccharide (LPS)-treated animals. The arginine synthesis was very sensitive to extracellular citrulline concentration in the range found in plasma (0.05-0.1 mM). The rate of arginine synthesis from citrulline was inhibited by about 20% by 0.5 mM-L-glutamine in both control and LPS-treated rat cells, but was inhibited by 0.5 mM-L-arginine only in control cells. Our results demonstrate that citrulline, produced by NO synthetase, can be recycled to arginine in macrophages. The citrulline-arginine cycle may contribute to the regulation of intracellular availability of arginine and thus the prolonged production of NO by macrophages.

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Citations
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Amino acids and immune function

TL;DR: Increasing evidence shows that dietary supplementation of specific amino acids to animals and humans with malnutrition and infectious disease enhances the immune status, thereby reducing morbidity and mortality.
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Arginine metabolism and nutrition in growth, health and disease

TL;DR: The results of both experimental and clinical studies indicate that Arg is a nutritionally essential amino acid (AA) for spermatogenesis, embryonic survival, fetal and neonatal growth, as well as maintenance of vascular tone and hemodynamics and novel and effective therapies for obesity, diabetes, and the metabolic syndrome.
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Molecular Biology of Mammalian Plasma Membrane Amino Acid Transporters

TL;DR: The tissue expression, transport characteristics, structure-function relationship, and the putative physiological roles of four amino acid transporters belonging to four protein families are described.
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New insights into the regulation of inducible nitric oxide synthesis

TL;DR: The roles NO plays in sepsis and the potential impact of arginine metabolism on NO synthesis are discussed and the only physiological nitrogen donor for NO synthesis, metabolism of this amino acid may play an important role in regulation of NO synthesis during sepsi.
References
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Journal ArticleDOI

Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor

TL;DR: NO released from endothelial cells is indistinguishable from EDRF in terms of biological activity, stability, and susceptibility to an inhibitor and to a potentiator.
Journal ArticleDOI

Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide.

TL;DR: The vascular effects of EDRF released from perfused bovine intrapulmonary artery and vein were compared with the effects of NO delivered by superfusion over endothelium-denuded arterial and venous strips arranged in a cascade to determine whether nitric oxide (NO) is responsible for the vascular smooth muscle relaxation elicited by endothelia-derived relaxing factor (EDRF).
Journal ArticleDOI

Vascular endothelial cells synthesize nitric oxide from L-arginine.

TL;DR: It is demonstrated that NO can be synthesized from L-arginine by porcine aortic endothelial cells in culture and the strict substrate specificity of this reaction suggests that L- arginine is the precursor for NO synthesis in vascular endothelium cells.
Journal ArticleDOI

Nitric oxide: a cytotoxic activated macrophage effector molecule.

TL;DR: The results suggest that nitric oxide is the precursor of nitrite/nitrate synthesized by cytotoxic activated macrophages and, via formation of iron-nitric oxide complexes and subsequent degradation of Iron-sulfur prosthetic groups, an effector molecule.
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