Chemical biology of nitric oxide: Regulation and protective and toxic mechanisms

Wink, David A.; Hanbauer, Ingeborg; Grisham, Matthew B.; Laval, Françoise; Nims, Raymond W.; Laval, Jacques; Cook, John A.; Pacelli, Roberto; Liebmann, James; Krishna, Murali C.; Ford, Peter C.; Mitchell, James B.

doi:10.1016/s0070-2137(96)80006-9

Cited by 261 publications

(151 citation statements)

References 103 publications

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“…To study the time requirements of cell exposure to NO, before proceeding to signaling studies, we used a panel of NO donors that differ in chemical characteristics and t 1/2 : SPER-NO and NOC-18, both nucleophile adducts of NO with t 1/2 of 39 min and 20 h, respectively (28,29), and GSNO and SNAP, S-nitrosothiols that generate nitrite at a steady rate over 30 -60 min (30,31). SPER-NO was the most rapidly acting, producing maximal inhibition of Ag-induced cytokine mRNA expression after only 2 h, while GSNO, SNAP, and NOC-18 produced maximal inhibition of cytokine mRNA at 4, 8, and 8 -24 h, respectively.…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Inhibits IgE-Dependent Cytokine Production and Fos and Jun Activation in Mast Cells

Davis

Flanagan

Gilfillan

et al. 2004

The Journal of Immunology

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NO is a cell-derived radical reported to inhibit mast cell degranulation and subsequent allergic inflammation, although whether its action is nonspecific or occurs via specific molecular mechanisms remains unknown. To examine this question, we set out to determine whether NO inhibits mast cell cytokine production, and, if so, whether it also alters FcεRI-dependent signal transduction. As hypothesized, the radical inhibited IgE/Ag-induced IL-4, IL-6, and TNF production. Although NO did not influence phosphorylated JNK, p38 MAPK, or p44/42 MAPK, it did inhibit phosphorylation of phospholipase Cγ1 and the AP-1 transcription factor protein c-Jun, but not NF-κB or CREB. NO further completely abrogated IgE/Ag-induced DNA-binding activity of the nuclear AP-1 proteins Fos and Jun. These results show that NO is capable of inhibiting FcεRI-dependent mast cell cytokine production at the level of gene regulation, and suggest too that NO may contribute to resolution of allergic inflammation.

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Section: Discussionmentioning

confidence: 99%

Nitric Oxide Inhibits IgE-Dependent Cytokine Production and Fos and Jun Activation in Mast Cells

Davis

Flanagan

Gilfillan

et al. 2004

The Journal of Immunology

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“…N 2 O 3 or ONOO -which can result in DNA lesions. The type of mutation under oxidative and nitrosative stresses differ [102]. Oxidative stress mediate DNA damage by the formation of peroxynitrile.…”

Section: Pro-tumor Effect Of Nomentioning

confidence: 99%

Biochemistry of Nitric Oxide

2011

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Nitric oxide (NO) a free radical having both cytoprotective as well as tumor promoting agent is formed from L-arginine by converting it to L-citrulline via nitric oxide synthase enzymes. The reaction product of nitric oxide with superoxide generates potent oxidizing agent, peroxynitrite which is the main mediator of tissue and cellular injury. Peroxynitrite is reactive towards many biomolecules which includes amino acids, nucleic acid bases; metal containing compounds, etc. NO metabolites may play a key role in mediating many of the genotoxic/ carcinogenic effects as DNA damage, protein or lipid modification, etc. The basic reactions of nitric oxide can be divided as direct effect of the radical where it alone plays a role in either damaging or protecting the cell milieu and an indirect effect in which the byproducts of nitric oxide formed by convergence of two independent radical generating pathways play the role in biological reactions which mainly involve oxidative and nitrosative stress. Nitric oxide is also capable of directly interacting with mitochondria through inhibition of respiration or by permeability transition. Reaction of nitric oxide with metal ions include its direct interaction with the metals or with oxo complexes thereby reducing them to lower valent state. Excessive production of nitric oxide can be studied by inhibiting the synthetic pathway of nitric oxide using both selective or specific nitric oxide synthase inhibitor or nonselective nitric oxide synthase inhibitor with respect to isoforms of nitric oxide.Keywords Nitric oxide Á Nitric oxide synthase Á Nitric oxide inhibitors Á Generation of nitric oxide Á Cancer Á Systemic lupus erythematosus Á Direct and indirect effect of nitric oxide Á Effect of nitric oxide on mitochondria

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“…It is a well-established fact that normal oxidative metabolism is a key endogenous generator of reactive oxygen (ROS) and nitrogen species (Wink et al, 1996;Adler et al, 1999;Finkel, 2000;Spitz et al, 2000). Furthermore, homeostatic control of normal cell growth pathways has been shown to be tightly dependent on oxidants (Burdon, 1996;Kamata and Hirata, 1999).…”

Section: Role Of Oxidative Metabolismmentioning

confidence: 99%

Oxidative metabolism, gap junctions and the ionizing radiation-induced bystander effect

2003

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Evidence accumulated over the past two decades has indicated that exposure of cell populations to ionizing radiation results in significant biological effects occurring in both the irradiated and nonirradiated cells in the population. This phenomenon, termed the 'bystander response', has been shown to occur both in vitro and in vivo and has been postulated to impact both the estimation of risks of exposure to low doses/low fluences of ionizing radiation and radiotherapy. Several mechanisms involving secreted soluble factors, oxidative metabolism and gapjunction intercellular communication have been proposed to regulate the radiation-induced bystander effect. Our current knowledge of the biochemical and molecular events involved in the latter two processes is reviewed in this article.

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Chemical biology of nitric oxide: Regulation and protective and toxic mechanisms

Cited by 261 publications

References 103 publications

Nitric Oxide Inhibits IgE-Dependent Cytokine Production and Fos and Jun Activation in Mast Cells

Nitric Oxide Inhibits IgE-Dependent Cytokine Production and Fos and Jun Activation in Mast Cells

Biochemistry of Nitric Oxide

Oxidative metabolism, gap junctions and the ionizing radiation-induced bystander effect

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