L‐arginine increases UVA cytotoxicity in irradiated human keratinocyte cell line: potential role of nitric oxide

Didier, Christine; Emonet‐Piccardi, Nathalie; Béani, J.-C.; Cadet, Jean; Richard, Marie‐Jeanne

doi:10.1096/fasebj.13.13.1817

Cited by 27 publications

(17 citation statements)

References 33 publications

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“…Since then, the interactions between SODs and ROS are being re-evaluated [85]. For example, exogenous SOD and L-thiocitrulline (an inhibitor of nitric oxide synthesis) prevented this cytotoxic effect, suggesting that the ratio of nitric oxide to superoxide radicals is important in UV-A-induced cytotoxicity [150]. Additionally, exogenous Cu-Zn SOD reduced the cell membrane injuries in UVB-irradiated murine fibroblast cells [151].…”

Section: Superoxide Dismutases (Sods)mentioning

confidence: 99%

Toxicity and Roles of Reactive Oxygen Species

Kimura

Sawada²,

Oshima³

et al. 2005

CDTIA

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The history of studies in biology regarding reactive oxygen species (ROS) is approximately 40 years. During the initial 30 years, it appeared that these studies were mainly focused on the toxicity or microbicidal-related agents of ROS. However, recent studies have identified another action regarding oxidative signaling, other than toxicity of ROS. Basically, it is suggested that ROS are reactive, and degenerate to biomacromolecules such as DNA and proteins, leading to deterioration of cellular functions as an oxidative stress. On the other hand, recent studies have shown that ROS act as oxidative signaling in cells, resulting in various gene expressions. For example, NADPH oxidase, a major source of superoxide radicals (O(2)(-)), expresses in various tissues such as leukocytes and cardiovascular systems, and ROS derived from the enzyme play important roles in cell proliferation, differentiation, and cell death. In this review, we have focused on and described the basic properties, toxicity, and roles of ROS.

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Section: Superoxide Dismutases (Sods)mentioning

confidence: 99%

Toxicity and Roles of Reactive Oxygen Species

Kimura

Sawada²,

Oshima³

et al. 2005

CDTIA

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“…whether caspase activation, PARP activity, and/or p38 MAP kinase activation are required for NO-induced death of NPC, we pretreated cells with a cell-permeant caspase inhibitor (zVAD-fmk), an inhibitor of PARP (3-aminobenzamide) (56,57), or an inhibitor of p38 MAP kinase (SB 203580) (58). Preliminary studies showed that none of the three inhibitors affected cell viability under basal culture conditions (data not shown).…”

Section: Activation Of Parp Caspases and P38 Map Kinase Are Each Rementioning

confidence: 99%

p38 MAP Kinase Mediates Nitric Oxide-induced Apoptosis of Neural Progenitor Cells

Cheng¹,

Chan²,

Milhavet³

et al. 2001

Journal of Biological Chemistry

143

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Neural progenitor cells (NPC) can proliferate, differentiate into neurons or glial cells, or undergo a form of programmed cell death called apoptosis. Although death of NPC occurs during development of the nervous system and in the adult, the underlying mechanisms are unknown. Here we show that nitric oxide (NO) can induce death of C17.2 NPC by a mechanism requiring activation of p38 MAP kinase, poly(ADP-ribose) polymerase, and caspase-3. Nitric oxide causes release of cytochrome c from mitochondria, and Bcl-2 protects the neural progenitor cells against nitric oxide-induced death, consistent with a pivotal role for mitochondrial changes in controlling the cell death process. Inhibition of p38 MAP kinase by SB203580 abolished NO-induced cell death, cytochrome c release, and activation of caspase-3, indicating that p38 activation serves as an upstream mediator in the cell death process. The antiapoptotic protein Bcl-2 protected NPC against nitric oxide-induced apoptosis and suppressed activation of p38 MAP kinase. The ability of nitric oxide to trigger death of NPC by a mechanism involving p38 MAP kinase suggests that this diffusible gas may regulate NPC fate in physiological and pathological settings in which NO is produced.

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“…UVA can also cause the production of reactive nitrogen species (e.g. nitric acid and peroxynitrite), which can cause cellular and DNA damage [8]. UVA predominantly induces oxidation of purines and of relatively few pyrimidines, as well as a few (single-)strand breaks in DNA [9][10][11].…”

Section: Dna Damagementioning

confidence: 99%

European Code against Cancer 4th Edition: Ultraviolet radiation and cancer

Greinert

Vries²,

Erdmann

et al. 2015

Cancer Epidemiology

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Ultraviolet radiation (UVR) is part of the electromagnetic spectrum emitted naturally from the sun or from artificial sources such as tanning devices. Acute skin reactions induced by UVR exposure are erythema (skin reddening), or sunburn, and the acquisition of a suntan triggered by UVR-induced DNA damage. UVR exposure is the main cause of skin cancer, including cutaneous malignant melanoma, basal-cell carcinoma, and squamous-cell carcinoma. Skin cancer is the most common cancer in fair-skinned populations, and its incidence has increased steeply over recent decades. According to estimates for 2012, about 100,000 new cases of cutaneous melanoma and about 22,000 deaths from it occurred in Europe. The main mechanisms by which UVR causes cancer are well understood. Exposure during childhood appears to be particularly harmful. Exposure to UVR is a risk factor modifiable by individuals' behaviour. Excessive exposure from natural sources can be avoided by seeking shade when the sun is strongest, by wearing appropriate clothing, and by appropriately applying sunscreens if direct sunlight is unavoidable. Exposure from artificial sources can be completely avoided by not using sunbeds. Beneficial effects of sun or UVR exposure, such as for vitamin D production, can be fully achieved while still avoiding too much sun exposure and the use of sunbeds. Taking all the scientific evidence together, the recommendation of the 4th edition of the European Code Against Cancer for ultraviolet radiation is: "Avoid too much sun, especially for children. Use sun protection. Do not use sunbeds."

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L‐arginine increases UVA cytotoxicity in irradiated human keratinocyte cell line: potential role of nitric oxide

Cited by 27 publications

References 33 publications

Toxicity and Roles of Reactive Oxygen Species

Toxicity and Roles of Reactive Oxygen Species

p38 MAP Kinase Mediates Nitric Oxide-induced Apoptosis of Neural Progenitor Cells

European Code against Cancer 4th Edition: Ultraviolet radiation and cancer

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