alexa The Metabolomics of Nitric Oxide and Reactive Nitrogen Species in Immune Editing Tumor Milieu: Influence of Nitric Oxide-Modulating Therapies
ISSN: 2157-7609

Journal of Drug Metabolism & Toxicology
Open Access

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Review Article

The Metabolomics of Nitric Oxide and Reactive Nitrogen Species in Immune Editing Tumor Milieu: Influence of Nitric Oxide-Modulating Therapies

Ashok R. Amin*
Department of Biochemical Engineering, Virginia Tech, Virginia College of Osteopathic Medicine. Rheumatrix Inc., Blacksburg, Virginia 24061, USA
Corresponding Author : Ashok R. Amin
Rheumatrix Inc., Blacksburg
Virginia 24060, USA
Tel: +908-416-5739
E-mail: [email protected]
Received January 13, 2012; Accepted July 06, 2012; Published July 09, 2012
Citation: Amin AR (2012) The Metabolomics of Nitric Oxide and Reactive Nitrogen Species in Immune Editing Tumor Milieu: Influence of Nitric Oxide-Modulating Therapies. J Drug Metab Toxicol S8:002. doi: 10.4172/2157-7609.S8-002
Copyright: © 2012 Amin AR, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Nitric oxide (NO), reactive nitrogen and oxygen species, hypoxia, L-arginine metabolites and peroxynitrite are contributing agents during various stages of carcinogenesis. Among these, NO contributes to various functions in the tumor microenvironment such as augmenting immune suppression, maintaining anergy to tumor associated antigens, stimulating angiogenesis, enhancing tumor growth and invasiveness, and modulating autophagy. Most cells in the tumor milieu either release NO and/or have altered physiological functions due to the influence of NO. Cancer cells evolve into a metabolic state to tolerate and reduce reactive nitrogen and oxygen species to elude oxidative damage. These cancer cells in the tumor microenvironment inhibit cellular infiltration of effector immune cells into the cancer milieu. Increased levels of CCAAT-enhancer-binding proteins such as C/EBP α and β are required for inducible Nitric Oxide Synthase (iNOS) gene expression and other transcripts for sustaining an immunosuppressive environment in growing tumors. The immunoediting property of reactive nitrogen and oxygen-modified metabolites change the functions of: intratumoral chemokines, T cell receptors, antigen specific tumor infiltrating lymphocytes (TILs), cytotoxic T lymphocyte, myeloid derived suppressive cells (MDSCs), gene expression, tumor suppressor genes, and Interferon responses which together countersignal tumor immunity. Recent studies show that reactive nitrogen species that promote tumor-mediated immune evasion can be reversed by gene therapy, immunotherapy, and chemotherapy by targeting or co-targeting excessive nitric oxide accumulation.

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