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493 results on '"Chignell, Colin F."'

13. Photorearrangement of alpha-azoxy ketones and triplet sensitization of azoxy compounds

Author

Engel, Paul S., Tsvaygboym, Konstantin P., Bachilo, Sergei, Smith, William B., Motten, Ann G., JinJie Jiang, and Chignell, Colin F.

Subjects
Excited state chemistry -- Research, Ketones -- Chemical properties, Radiation chemistry -- Research, Biological sciences, Chemistry
Abstract

A report on the generation of alpha-azoxy radicals under mild conditions by irradiation of alpha-azoxy ketones is presented. Azoxy compounds are also found to be good quenchers of triplet excited acetophenone.

Published
2005

15. The pH-dependent primary photoreactions of ochratoxin A

Author

Il'ichev, Yuri V., Perry, Jennifer L., Manderville, Richard A., Chignell, Colin F., and Simon, John D.

Subjects
Chemistry, Physical and theoretical -- Research, Hydrogen-ion concentration -- Physiological aspects, Toxins -- Physiological aspects, Ethers -- Physiological aspects, DNA -- Research, Chemicals, plastics and rubber industries
Published
2001

32. Oxidation of aci-nitromethane by singlet oxygen in aqueous solution

Author

Bilski, Piotr, Reszka, Krzysztof, and Chignell, Colin F.

Subjects
Oxidation-reduction reaction -- Analysis, Methane -- Research, Photochemical research -- Observations, Chemistry
Abstract

The aci tautomer of nitromethane (NM) quenches (1)O(2) phosphorescence on addition of (1)O(2) with a high quantum yield of oxygen photo consumption. Decomposition of the aci-nitro group proceeds through peroxy intermediates and nitrogen peroxides, with formate and nitrate as the major oxidation products. Singlet oxygen reacts with the carbon atom in the NM, yielding a biradical intermediate that undergoes decomposition, faster than cyclization, to form an ozonide transient. The quantum yield of oxygen photo consumption by aci-NM is enhanced by a higher concentration of NM in NaOH solution.

Published
1994

33. EPR and spin-trapping investigation of free radicals from the reaction of 4-methoxybenzenediazonium tetrafluoroborate with melanin and melanin precursors

Author

Reszka, Krzysztof J. and Chignell, Colin F.

Subjects
Electron paramagnetic resonance -- Usage, Melanin -- Research, Free radicals (Chemistry) -- Physiological aspects, Chemistry
Abstract

EPR spectroscopy and spin-trapping method were used to examine the interaction of synthetic 3,4-dihydroxyphenylalanine (DOPA) melanin (DM) and its precursors, with 4-methoxybenzenediazonium tetrafluoroborate, 4-MeO-PhN2BF4. A one electron-transfer mechanism facilitates the reaction of DM, catechol, 3,4-dihydroxybenzoic acid, 3,4-dihydroxyhydrocinnamic acid, 3, 4-dihydroxyphenylalanine, and 6-hydroxydopamine with 4-MeO-PhN2+. Hydroquinones and semiquinone radicals enhanced the homolysis of diazonium salts to produce aryl radicals.

Published
1993

49. UVA-induced cell cycle progression is mediated by ADAM/EGFR/AKT/Cyclin D1 pathways in keratinocytes

Author

He, Yu-Ying, Council, Sarah E., Feng, Li, and Chignell, Colin F.

Subjects
Keratinocytes, Skin Neoplasms, Ultraviolet Rays, Cell Cycle, Antineoplastic Agents, ADAM17 Protein, Models, Biological, Article, ErbB Receptors, ADAM Proteins, Phosphatidylinositol 3-Kinases, Cell Line, Tumor, Humans, Cyclin D1, sense organs, Enzyme Inhibitors, Proto-Oncogene Proteins c-akt, Cell Proliferation
Abstract

UVA (315-400 nm), which constitutes approximately 95% of the UV irradiation in natural sunlight, represents a major environmental challenge to the skin and is clearly associated with human skin cancer. Here, we show that a low, nonlethal dose of UVA induces dose-dependent cell cycle progression in human HaCaT keratinocytes. We found that UVA induced cyclin D1 accumulation, whereas siRNA knockdown of cyclin D1 blocked the UVA-induced cell cycle progression, indicating that this process is mediated by cyclin D1. UVA irradiation also induced AKT activation; when cells were incubated with phosphatidylinositol-3-OH kinase/AKT inhibitor or infected with dominant-negative AKT, cyclin D1 up-regulation, cell cycle progression, and proliferation were inhibited, suggesting that AKT activation is required for UVA-induced cell cycle progression. In contrast, extracellular signal-regulated kinase (ERK) was not activated by UVA exposure; incubation with ERK/mitogen-activated protein kinase inhibitor had no effect on UVA-induced cyclin D1 up-regulation and cell cycle progression. Activation of epidermal growth factor receptor (EGFR) was observed after UVA exposure. EGFR kinase inhibitor AG attenuated the UVA-induced AKT/cyclin D1 pathway and cell cycle progression, indicating that EGFR is upstream of AKT/cyclin D1 pathway activation. Furthermore, metalloprotease inhibitor GM6001 blocked UVA-induced cell cycle progression, and siRNA knockdown of a disintegrin and metalloprotease (ADAM)17 had a similar inhibitory effect, demonstrating that ADAM17 mediates the EGFR/AKT/cyclin D1 pathway and cell cycle progression to the S phase induced by UVA radiation. Identification of these signaling pathways in UVA-induced cell proliferation will facilitate the development of efficient and safe chemopreventive and therapeutic strategies for skin cancer.

Published
2008

50. Phototoxicity in Human Retinal Pigment Epithelial Cells Promoted by Hypericin, a Component of St. John’s Wort†

Author

Wielgus, Albert R., Chignell, Colin F., Miller, David S., Van Houten, Ben, Meyer, Joel, Hu, Dan-Ning, and Roberts, Joan E.

Subjects
Anthracenes, Male, Light, Cell Survival, Middle Aged, Glutathione, Article, Humans, Lipid Peroxidation, Pigment Epithelium of Eye, Oxidation-Reduction, Perylene, Cells, Cultured, Hypericum
Abstract

St. John's wort (SJW), an over-the-counter antidepressant, contains hypericin, which absorbs light in the UV and visible ranges. In vivo studies have determined that hypericin is phototoxic to skin and our previous in vitro studies with lens tissues have determined that it is potentially phototoxic to the human lens. To determine if hypericin might also be phototoxic to the human retina, we exposed human retinal pigment epithelial (hRPE) cells to 10(-7) to 10(-5) M hypericin. Fluorescence emission detected from the cells (lambda(ex) = 488 nm; lambda(em) = 505 nm) confirmed hypericin uptake by human RPE. Neither hypericin exposure alone nor visible light exposure alone reduced cell viability. However when irradiated with 0.7 J cm(-2) of visible light (lambda400 nm) there was loss of cell viability as measured by MTS and lactate dehydrogenase assays. The presence of hypericin in irradiated hRPE cells significantly changed the redox equilibrium of glutathione and a decrease in the activity of glutathione reductase. Increased lipid peroxidation as measured by the thiobarbituric acid reactive substances assay correlated to hypericin concentration in hRPE cells and visible light radiation. Thus, ingested SJW is potentially phototoxic to the retina and could contribute to retinal or early macular degeneration.

Published
2007

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