Nitric oxide. A macrophage product responsible for cytostasis and respiratory inhibition in tumor target cells.
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- D J Stuehr
- Beatrice and Samuel A. Seaver Laboratory, Department of Medicine, Cornell University Medical College, New York, New York 10021.
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- C F Nathan
- Beatrice and Samuel A. Seaver Laboratory, Department of Medicine, Cornell University Medical College, New York, New York 10021.
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<jats:p>A metabolic pathway of activated macrophages (M phi) involving oxidation of the guanido nitrogens of L-arginine is required for inhibition of growth and respiration of some target cells. The goal of this study was to identify the M phi metabolite(s) that induce these injuries. The stable products of the L-arginine pathway, NO2- and NO3-, were incapable of causing cytostasis under coculture conditions. However, NO2- became cytostatic upon mild acidification, which favors its transformation into nitrogen oxides of greater reactivity. This suggested that NO. (and/or NO2), recently identified as an M phi metabolite of L-arginine, could be a mediator. Authentic NO. caused cytostasis and respiratory inhibition in L1210 cells in a dose-dependent manner. The mitochondrial lesions caused by NO. were confined to complex 1 and 2, a pattern of injury identical to that seen after coculture with activated M phi. Inclusion of NO. scavenger systems prevented cytostasis from developing in M phi-L1210 cocultures. Thus, M phi-generated NO. can account for L-arginine-dependent cytostasis and respiratory inhibition.</jats:p>
収録刊行物
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- The Journal of experimental medicine
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The Journal of experimental medicine 169 (5), 1543-1555, 1989-05-01
Rockefeller University Press
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詳細情報
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- CRID
- 1364233270670748672
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- NII論文ID
- 80004613983
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- NII書誌ID
- AA00697559
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- ISSN
- 15409538
- 00221007
- http://id.crossref.org/issn/00221007
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