Peroxynitrite-Induced Apoptosis in Epithelial (T84) and Macrophage (RAW 264.7) Cell Lines: Effect of Legume-Derived Polyphenols (Phytolens)

Sandoval, Manuel; Ronzio, Robert A.; Muanza, Dave N.; Clark, David A.; Miller, Mark J.S.

doi:10.1006/niox.1997.0160

Cited by 33 publications

(25 citation statements)

References 33 publications

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“…114,115 Macrophage apoptosis can also be induced by exposure to ONOO À , via oxidative stress, which can be reduced by antioxidants such as ascorbic acid or phytolens. 30,116 Induction of apoptosis by NO in elicited murine macrophages or RAW 264.7 cells has also been attributed to the formation of ONOO À within mitochondria, as nitrotyrosine residues were detected in cytochrome c. 23 ONOO À and metabolites of NO (e.g. N 2 O 3 ) can cause direct DNA damage or inhibit DNA repair enzymes, 117 leading to an increase in the tumour suppressor protein p53, which has been shown to accumulate in NO-treated macrophages and may be the factor responsible for driving them towards apoptosis.…”

Section: Proapoptotic Mechanismsmentioning

confidence: 99%

Nitric oxide: a key regulator of myeloid inflammatory cell apoptosis

et al. 2003

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Apoptosis of inflammatory cells is a critical event in the resolution of inflammation, as failure to undergo this form of cell death leads to increased tissue damage and exacerbation of the inflammatory response. Many factors are able to influence the rate of apoptosis in neutrophils, eosinophils, monocytes and macrophages. Among these is the signalling molecule nitric oxide (NO), which possesses both anti-and proapoptotic properties, depending on the concentration and flux of NO, and also the source from which NO is derived. This review summarises the differential effects of NO on inflammatory cell apoptosis and outlines potential mechanisms that have been proposed to explain such actions.

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Section: Proapoptotic Mechanismsmentioning

confidence: 99%

Nitric oxide: a key regulator of myeloid inflammatory cell apoptosis

et al. 2003

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“…The precise role of ONOO -in inflammatory cell apoptosis remains to be elucidated. There is some evidence to suggest that at high concentrations (100 µM -300 µM), ONOO -induces apoptosis in RAW 264.7 cells [68], whilst at lower concentrations (30 µM -50 µM), it may have a protective effect against lipopolysaccharide (LPS) and interferon (IFN)-γ-induced apoptosis in these cells [69]. Brockhaus et al [70] have demonstrated that overexpression of copper/zinc SOD (CuZnSOD) can protect RAW 264.7 cells against apoptosis initiated by NO, either exogenous or iNOS-derived.…”

Section: No As a Mediator Of Apoptosismentioning

confidence: 98%

Apoptosis and Atherosclerosis: The Role of Nitric Oxide

Shaw¹,

Megson²,

Rossi³

2006

AIAAMC

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Atherosclerosis, and its associated complications, are a major cause of morbidity and mortality, and it is now recognised as a chronic inflammatory disorder. Progression of inflammation depends on the balance between recruitment of inflammatory cells and their subsequent removal from a site of inflammation. Apoptosis, or programmed cell death, is a fundamental process governing cell survival and is a major determinant of the resolution of the inflammatory response. Apoptotic cells are instantly recognised for non-inflammatory clearance by phagocytes (e.g. macrophages) and removed from the vicinity of inflammation without the release of their pro-inflammatory cell contents. Nitric oxide (NO) plays an important role in many biological processes and has several anti-atherogenic properties including vasodilatation, inhibition of platelet activation and aggregation, and the regulation of apoptosis in a variety of cell types involved in atherogenesis. A critical early event during atherogenesis is injury to the endothelium. The ensuing damage results in endothelial dysfunction, including a reduction in the capacity of the endothelium to generate NO. Decreased NO bioavailability is likely to influence many cellular processes occurring within atherosclerotic lesions, including apoptosis. Modulation of apoptosis is a novel target for therapeutic intervention in the treatment of chronic inflammatory disorders, such as atherosclerosis. This modulation may help limit or resolve inflammation without the concomitant recruitment of subsequent inflammatory cells, thereby reducing the potential for further tissue damage. NO is a possible candidate for manipulation of atherosclerotic processes due to both its powerful anti-atherogenic characteristics and ability to affect apoptosis. This review highlights the role of apoptosis in atherosclerosis and discusses the therapeutic potential of NO to limit and/or resolve vascular inflammation.

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“…It also readily forms damaging RNIs. For example, with superoxide it will form peroxynitrate, a known inducer of apoptosis (Sandoval et al 1997;Brockhaus and Brune 1999;Szabo 2003) and reactions with thiols and transition metal complexes form S-nitrosothiols (SNOs) and metal-nitrosyl adducts, respectively. Nitrate and met-haemoglobin (met-Hb), SNO-Hb or iron-nitrosyl Hb can be formed when NO reacts with partially oxygenated haemoglobin.…”

Section: Signals That Induce Parasite Apoptosismentioning

confidence: 99%