The presence of nitrite during UVA irradiation protects from apoptosis

Suschek, Christoph V.; Schröeder, Peter; Aust, Olivier; Sies, Helmut; Mahotka, Csaba; Horstjann, Markus; Ganser, Heiko; Mürtz, Manfred; Hering, P.; Schnorr, Oliver; Kröncke, Klaus‐Dietrich; Kolb-Bachofen, Victoria

doi:10.1096/fj.03-0359fje

Cited by 39 publications

(22 citation statements)

References 34 publications

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“…In the present study, 10 mM nitrite showed a trend of cell accumulation in the G 0 /G 1 phase, as was observed previously at low sodium nitrite concentrations (up to 6.25 mM), whereas higher concentrations reduced the cell proliferation in the human gastric adenocarcinoma epithelial cell line (Sun et al, 2006). In another study on endothelial cells, the presence of nitrite (10 mM), but not nitrate, during UV irradiation of cells exerted a potent and concentration-dependent protection against apoptotic cell death, because of the photodecomposition of nitrite to generate NO (Suschek et al, 2003). BrdU incorporation confirmed the nitrite-mediated increase in S phase.…”

Section: Discussionsupporting

confidence: 78%

“…Nitrite therapy significantly augmented vascular density in the ischemic limbs by inducing endothelial cell proliferation and angiogenesis (Kumar et al, 2008); however, underlying mechanisms were not investigated. Nitrite also prevented endothelial cell apoptosis after UV exposure (Suschek et al, 2003). Oral administration of sodium nitrite (25-100 mg/kg) reduced lymphocytes, but augmented circulating neutrophils in BALB/c mice (Abuharfeil et al, 2001).…”

Section: Introductionmentioning

confidence: 89%

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Nitrite-Mediated Modulation of HL-60 Cell Cycle and Proliferation: Involvement of Cyclin-Dependent Kinase 2 Activation

Kumar

Barthwal²,

Dikshit³

2011

J Pharmacol Exp Ther

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Recent research suggests the vivid possibility of using nitrite therapy against various pathological conditions. Moreover, chronic nitrite therapy offers protection against ischemia and augments endothelial cell proliferation through unknown mechanisms. Nitrite-mediated augmentation in the number of circulating neutrophils has also been reported; however, the exact mechanism is not known. In the present study, we have investigated the effect of nitrite (0.5-10 mM) on the proliferation of the neutrophilic cell line HL-60 and also explored the underlying mechanism. Treatment of HL-60 cells with sodium nitrite (0.5-5 mM) led to an increase in cell proliferation, which was confirmed by cell cycle analysis and 5-bromo-2-deoxyuridine and thymidine incorporation, whereas cells accumulated in the G 0 /G 1 phase after treatment with 10 mM nitrite. Experiments on the synchronized cells exhibited similar effect, which seems to be nitric oxide (NO)-dependent, because carboxyl-1H-imidazol-1-yloxy,2-(4-carboxyphenyl)-4,5-dihydro 4,4,5,5-tetramethyl-3-oxide abolished nitrite-mediated proliferative effect. Moreover, the NO donor sodium nitroprusside at micromolar concentrations also exhibited similar effects. Nitrite induced augmentation in S phase, and intracellular reactive oxygen species (ROS) generation was prevented by ROS scavenger/inhibitors. Moreover, mitochondrial blockers, rotenone and antimycin A, also reduced nitrite-mediated cell proliferation. Assessment of the cell cycle regulators cyclin-dependent kinase 2 (Cdk2), Cdk4, cyclin A, cyclin D, cyclin E, and p21 suggested augmentation in the expression and interaction of Cdk2/cyclin E and Cdk2 activity, whereas p21 was down-regulated. Indeed proliferative effect of nitrite was blocked by roscovitine, a Cdk2 inhibitor. The results obtained demonstrate that the proliferative effect of nitrite on HL-60 cells seems to be NO-mediated, redox-sensitive, and Cdk2 activation-dependent, warranting detailed studies before initiating its clinical use.

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Section: Discussionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 89%

Nitrite-Mediated Modulation of HL-60 Cell Cycle and Proliferation: Involvement of Cyclin-Dependent Kinase 2 Activation

Kumar

Barthwal²,

Dikshit³

2011

J Pharmacol Exp Ther

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“…In our study, nitrite but not the mitochondrial-targeted antioxidant Mito-TEMPO influenced TNF-α/CHX-induced decrease in cell viability of MODE-K cells. The concentration of nitrite (10 mM) used was shown to provide complete rescue of UVA-induced apoptotic cell death in rat aortic endothelial cells [61]. We also found that nitrite reduced TNF-α/CHX-induced caspase-3/7 activation.…”

Section: Influence Of Antioxidant Related Products On Tnf-α/chx-inducsupporting

confidence: 51%

TNF-α/Cycloheximide-Induced Oxidative Stress and Apoptosis in Murine Intestinal Epithelial MODE-K Cells

Babu

Soenen²,

Raemdonck³

et al. 2012

CPD

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In the mouse postoperative ileus model, we have shown an increase in oxidative stress after intestinal manipulation occurring earlier in the mucosa than in the muscular layer, which might contribute to epithelial barrier dysfunction. To address these findings in vitro, we assessed TNF-α/cycloheximide (CHX)-induced oxidative stress and apoptosis in a mouse intestinal epithelial cell line, MODE-K. The influence of heme oxygenase (HO)-1-related products and agents known to reduce reactive oxygen species (ROS) production on TNF-α/CHX-induced oxidative stress and apoptosis were investigated. MODE-K cells were exposed to different concentrations of TNF-α/CHX in the absence/presence of the test agents.Cell viability, caspase-3/7 activity, apoptosis, reduced glutathione level (GSH) and intracellular ROS production were measured. TNF-α/CHX decreased cell viability, increased caspase-3/7 activity, induced apoptosis, reduced the GSH level and increased ROS production in a concentration-dependent manner in MODE-K cells. All these effects of TNF-α/CHX were partially prevented by pretreatment with a carbon monoxide-releasing agent (CORM-A1) and nitrite. The antioxidant resveratrol abolished TNF-α/CHX-induced increase in ROS production and caspase-3/7 activity, but apoptosis was only partially prevented. MODE-K cells are sensitive to TNF-α-induced apoptosis in the presence of CHX, which is associated with increased intracellular ROS production and caspase-3/7 activation. The effects were partially mitigated by CORM-A1, nitrite and resveratrol. Thus, these agents could be of potential use in protecting the epithelial barrier against oxidative stress during intestinal ischemia/reperfusion injury.

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“…For example, the content of nitrite in sweat, covering skin, could provide benefit, because there is generation of NO from nitrite under UVA radiation (153). NO is a signaling molecule involved in UVB-induced melanogenesis (134).…”

Section: Discussionmentioning

confidence: 99%

Nutritional Protection Against Skin Damage From Sunlight

2004

Self Cite

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▪ Abstract The concept of systemic photoprotection by dietary means is gaining momentum. Skin is continuously exposed to ultraviolet (UV) radiation, the major cause of skin disorders such as sunburn, photodamage, and nonmelanoma skin cancer. Most of the erythemal annual UV dose is encountered under nonvacation conditions, when no sunscreen is applied. In the absence of topically added compounds, skin protection depends solely on endogenous defense. Micronutrients can act as UV absorbers, as antioxidants, or can modulate signaling pathways elicited upon UV exposure. UV-induced erythema is a suitable parameter to assess photoprotection. Dietary protection is provided by carotenoids, tocopherols, ascorbate, flavonoids, or n-3 fatty acids, contributing to maintenance resistance as part of lifelong protection.

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The presence of nitrite during UVA irradiation protects from apoptosis

Cited by 39 publications

References 34 publications

Nitrite-Mediated Modulation of HL-60 Cell Cycle and Proliferation: Involvement of Cyclin-Dependent Kinase 2 Activation

Nitrite-Mediated Modulation of HL-60 Cell Cycle and Proliferation: Involvement of Cyclin-Dependent Kinase 2 Activation

TNF-α/Cycloheximide-Induced Oxidative Stress and Apoptosis in Murine Intestinal Epithelial MODE-K Cells

Nutritional Protection Against Skin Damage From Sunlight

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The presence of nitrite during UVA irradiation protects from apoptosis

Cited by 39 publications

References 34 publications

Nitrite-Mediated Modulation of HL-60 Cell Cycle and Proliferation: Involvement of Cyclin-Dependent Kinase 2 Activation

Nitrite-Mediated Modulation of HL-60 Cell Cycle and Proliferation: Involvement of Cyclin-Dependent Kinase 2 Activation

TNF-&alpha;/Cycloheximide-Induced Oxidative Stress and Apoptosis in Murine Intestinal Epithelial MODE-K Cells

Nutritional Protection Against Skin Damage From Sunlight

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TNF-α/Cycloheximide-Induced Oxidative Stress and Apoptosis in Murine Intestinal Epithelial MODE-K Cells