Nitric Oxide: A New Paradigm for Second Messengers

Kerwin, James F.; Lancaster, Jack R.; Feldman, Paul L.

doi:10.1021/jm00022a001

Cited by 564 publications

(536 citation statements)

References 73 publications

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“…As the structure and function of these enzymes have been reviewed extensively in the past few years (e.g. [36,[280][281][282]), only selected features of these enzymes will be noted here. Briefly, there are three NOS isoenzymes, encoded by distinct genes : iNOS (Type II NOS), neuronal NOS (nNOS ; Type I NOS) and eNOS (Type III NOS).…”

Section: Nosmentioning

confidence: 99%

Arginine metabolism: nitric oxide and beyond

Morris

1998

Biochemical Journal

2,424

2,036

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Arginine is one of the most versatile amino acids in animal cells, serving as a precursor for the synthesis not only of proteins but also of nitric oxide, urea, polyamines, proline, glutamate, creatine and agmatine. Of the enzymes that catalyse rate-controlling steps in arginine synthesis and catabolism, argininosuccinate synthase, the two arginase isoenzymes, the three nitric oxide synthase isoenzymes and arginine decarboxylase have been recognized in recent years as key factors in regulating newly identified aspects of arginine metabolism. In particular, changes in the activities of argininosuccinate synthase, the arginases, the inducible isoenzyme of nitric oxide synthase and also cationic amino acid transporters play major roles in determining the metabolic fates of arginine in health and disease, and recent studies have identified

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Section: Nosmentioning

confidence: 99%

Arginine metabolism: nitric oxide and beyond

Morris

1998

Biochemical Journal

2,424

2,036

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“…In addition to its functions as a messenger molecule (acting through the heinemediated stimulation of soluble guanylyl cyclase [3]), *NO is paramagnetic and reacts with metals and with oxygen species [4]. There is much data to suggest that the interaction of • NO with oxygen species can affect oxidative injury, although the actions of •NO can be to either attenuate or potentiate injury.…”

Section: Introductionmentioning

confidence: 99%

“…The factors which determine this 'Janus-faced' action of *NO [5] are largely unknown. Much of the contradictory data on the damaging vs. protective actions of NO synthesis may be due to the multiple nitrogen oxide species which are produced in the aerobic, chemically complex biological milieu [4] and it is difficult to ascribe a particular biological effect to a specific derivative of NO.…”

Section: Introductionmentioning

confidence: 99%

Nitrogen oxide‐induced autoprotection in isolated rat hepatocytes

Kim

Bergonia

Lancaster³

1995

FEBS Letters

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197

110

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Pretreatment of rat hepatocytes with low-dose nitrogen oxide (addition of SNAP in vitro or induction of nitric oxide synthase in vitro or in vivo) imparts resistance to killing and decrease in aconitase and mitochondrial electron transfer from a second exposure to a higher dose of SNAP. Induction of this resistance is prevented by cycloheximide, indicating upregulation of protective protein(s). Ferritin levels are increased as are nonheme iron-NO EPR signals. Tin-protoporphyrin (SnPP) prevents protection, suggesting involvement of hsp32 (heme oxygenase) and/or guanylyl cyclase (GC). Cross-resistance to H2Oz killing is also observed, which is also prevented by cycloheximide and SnPP. Thus, hepatocytes possess inducible protective mechanisms against nitrogen oxide and reactive oxygen toxicity.

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“…[1][2][3] Interestingly, cancer cells show peculiar mitochondrial dysfunctions that can be harnessed for selectivet oxicity,w ith respect to normaltransformed cells. [4,5] Nitric oxide (NO), au biquitous messenger which plays important roles in many physiological and pathological processes, [6,7] exerts profound effects on mitochondria. Within these organelles, it may either originate from an itric oxide synthase (NOS) isoform, anchored to the cytosolic face of the outer mitochondrialm embrane, or,p ossibly,f rom am itochondrial NOS located inside mitochondria.…”

Section: Introductionmentioning

confidence: 99%

A Molecular Hybrid for Mitochondria‐Targeted NO Photodelivery

et al. 2017

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The design, synthesis, spectroscopic and photochemical properties, and biological evaluation of a novel molecular hybrid that is able to deliver nitric oxide (NO) into mitochondria are reported. This molecular conjugate unites a tailored o‐CF3‐p‐nitroaniline chromophore, for photo‐regulated NO release, and a rhodamine moiety, for mitochondria targeting, in the same molecular skeleton via an alkyl spacer. A combination of steady‐state and time‐resolved spectroscopic and photochemical experiments demonstrate that the two chromogenic units preserve their individual photophysical and photochemical properties in the conjugate quite well. Irradiation with violet light triggers NO release from the nitroaniline moiety and photoionization in the rhodamine center, which also retains considerable fluorescence efficiency. The molecular hybrid preferentially accumulates in the mitochondria of A549 lung adenocarcinoma cells where it induces toxicity at a concentration of 1 μm, exclusively upon irradiation. Comparative experiments, carried out with ad‐hoc‐synthesized model compounds, suggest that the phototoxicity observed at such a low concentration is probably not due to NO itself, but rather to the formation of the highly reactive peroxynitrite that is generated from the reaction of NO with the superoxide anion.

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Nitric Oxide: A New Paradigm for Second Messengers

Cited by 564 publications

References 73 publications

Arginine metabolism: nitric oxide and beyond

Arginine metabolism: nitric oxide and beyond

Nitrogen oxide‐induced autoprotection in isolated rat hepatocytes

A Molecular Hybrid for Mitochondria‐Targeted NO Photodelivery

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