WordNet

urge on; cause to act; "The other children egged the boy on, but he did not want to throw the stone through the window" (同)incite, egg on
a pointed instrument that is used to prod into a state of motion (同)goad
in favor of a proposition, opinion, etc.
an argument in favor of a proposal
in favor of (an action or proposal etc.); "a pro vote"
a substance that oxidizes another substance (同)oxidizer, oxidiser, oxidizing_agent

PrepTutorEJDIC

突き刺す(つつく)こと / 刺し針,突き棒 / (一般に)刺激 / (先のとがったもので)…‘を'突き刺す,つつく《+『名』+『with』+『名』》 / …‘を'刺激する,呼び起こす;〈人〉‘を'励まして(…を)促す《+『名〈人〉+『to』(『into』)+『名』(do『ing』)》 / (…を)突く,つつく《+『at』+『名』》
=professional
賛成論;賛成票(者) / 賛成して
オキシダント,酸化体
Public Relations Officer 広報活動員,宣伝担当者

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/04/17 16:15:49」(JST)

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Pro-oxidants are chemicals that induce oxidative stress, either by generating reactive oxygen species or by inhibiting antioxidant systems.^[1] The oxidative stress produced by these chemicals can damage cells and tissues, for example an overdose of the analgesic paracetamol (acetaminophen) can fatally damage the liver, partly through its production of reactive oxygen species.^[2]^[3]

Some substances can serve as either antioxidants or pro-oxidants, depending on conditions.^[4] Some of the conditions that are important include the concentration of the chemical and if oxygen or transition metals are present. While thermodynamically very favored, reduction of molecular oxygen or peroxide to superoxide or hydroxyl radical is fortunately spin forbidden. This greatly reduces the rates of these reactions, thus allowing aerobic life to exist. As a result, the reduction of oxygen typically involves either the initial formation of singlet oxygen, or spin-orbit coupling through a reduction of a transition-series metal such as manganese, iron, or copper. This reduced metal then transfers the single electron to molecular oxygen or peroxide.

Metals

Transition metals can serve as pro-oxidants. For example, chronic manganism is a classic "pro-oxidant" disease.^[5] Another disease associated with the chronic presence of a pro-oxidant transition-series metal is hemochromatosis, associated with elevated iron levels. Similarly, Wilson's disease is associated with elevated tissue levels of copper. Such syndromes tend to be associated with a common symptomology. Thus, all are occasional symptoms of (e.g) hemochromatosis, another name for which is "bronze diabetes". The pro-oxidant herbicide paraquat, Wilson's disease, and striatal iron have similarly been linked to human Parkinsonism. Paraquat also produces parkinsonian-like symptoms in rodents.

Fibrosis

Fibrosis or scar formation is another pro-oxidant-related symptom. E.g., interocular copper or vitreous chalcosis is associated with severe vitreous fibrosis, as is interocular iron. Liver cirrhosis is also a major symptom of Wilson's disease. The pulmonary fibrosis produced by paraquat and the antitumor agent bleomycin is also thought to be induced by the pro-oxidant properties of these agents. It may be that oxidative stress produced by such agents mimics a normal physiological signal for fibroblast conversion to myofibroblasts.

Pro-oxidant vitamins

Vitamins that are reducing agents can be pro-oxidants. Vitamin C has antioxidant activity when it reduces oxidizing substances such as hydrogen peroxide,^[6] however, it can also reduce metal ions which leads to the generation of free radicals through the fenton reaction.^[7]^[8]

2 Fe²⁺ + 2 H₂O₂ → 2 Fe³⁺ + 2 OH· + 2 OH⁻

2 Fe³⁺ + Ascorbate → 2 Fe²⁺ + Dehydroascorbate

The metal ion in this reaction can be reduced, oxidized, and then re-reduced, in a process called redox cycling that can generate reactive oxygen species.

The relative importance of the antioxidant and pro-oxidant activities of antioxidant vitamins are an area of current research, but vitamin C, for example, appears to have a mostly antioxidant action in the body.^[7]^[9] However, less data is available for other dietary antioxidants, such as polyphenol antioxidants,^[10] zinc,^[11] and vitamin E.^[12]

Anticancer Drugs

Several important anticancer agents both bind to DNA and generate reactive oxygen species. These include adriamycin and other anthracyclines, bleomycin, and cisplatin. These agents may show specific toxicity towards cancer cells because of the low level of antioxidant defenses found in tumors. Recent research demonstrates that redox dysregulation originating from metabolic alterations and dependence on mitogenic and survival signaling through reactive oxygen species represents a specific vulnerability of malignant cells that can be selectively targeted by pro-oxidant non-genotoxic redox chemotherapeutics.^[13]

References

^ Puglia CD, Powell SR (1984). "Inhibition of cellular antioxidants: a possible mechanism of toxic cell injury". Environ. Health Perspect. 57: 307–11. doi:10.2307/3429932. JSTOR 3429932. PMC 1568295. PMID 6094175.
^ James LP, Mayeux PR, Hinson JA (2003). "Acetaminophen-induced hepatotoxicity". Drug Metab. Dispos. 31 (12): 1499–506. doi:10.1124/dmd.31.12.1499. PMID 14625346.
^ Jaeschke H, Gores GJ, Cederbaum AI, Hinson JA, Pessayre D, Lemasters JJ (2002). "Mechanisms of hepatotoxicity". Toxicol. Sci. 65 (2): 166–76. doi:10.1093/toxsci/65.2.166. PMID 11812920.
^ Herbert V (1996). "Prooxidant effects of antioxidant vitamins. Introduction". J. Nutr. 126 (4 Suppl): 1197S–200S. PMID 8642456.
^ Han SG, Kim Y, Kashon ML, Pack DL, Castranova V, Vallyathan V (December 2005). "Correlates of oxidative stress and free-radical activity in serum from asymptomatic shipyard welders". Am. J. Respir. Crit. Care Med. 172 (12): 1541–8. doi:10.1164/rccm.200409-1222OC. PMID 16166614.
^ Duarte TL, Lunec J (2005). "Review: When is an antioxidant not an antioxidant? A review of novel actions and reactions of vitamin C". Free Radic. Res. 39 (7): 671–86. doi:10.1080/10715760500104025. PMID 16036346.
^ ^a ^b Carr A, Frei B (1 June 1999). "Does vitamin C act as a pro-oxidant under physiological conditions?". FASEB J. 13 (9): 1007–24. PMID 10336883.
^ Stohs SJ, Bagchi D (1995). "Oxidative mechanisms in the toxicity of metal ions". Free Radic. Biol. Med. 18 (2): 321–36. doi:10.1016/0891-5849(94)00159-H. PMID 7744317.
^ Valko M, Morris H, Cronin MT (2005). "Metals, toxicity and oxidative stress". Curr. Med. Chem. 12 (10): 1161–208. doi:10.2174/0929867053764635. PMID 15892631.
^ Halliwell B (2007). "Dietary polyphenols: good, bad, or indifferent for your health?". Cardiovasc. Res. 73 (2): 341–7. doi:10.1016/j.cardiores.2006.10.004. PMID 17141749.
^ Hao Q, Maret W (2005). "Imbalance between pro-oxidant and pro-antioxidant functions of zinc in disease". J. Alzheimers Dis. 8 (2): 161–70; discussion 209–15. PMID 16308485.
^ Schneider C (2005). "Chemistry and biology of vitamin E". Mol Nutr Food Res 49 (1): 7–30. doi:10.1002/mnfr.200400049. PMID 15580660.
^ Wondrak GT (December 2009). "Redox-directed cancer therapeutics: molecular mechanisms and opportunities". Antioxid. Redox Signal. 11 (12): 3013–69. doi:10.1089/ARS.2009.2541. PMC 2824519. PMID 19496700.

UpToDate Contents

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1. 心不全におけるナトリウム利尿ペプチド測定 natriuretic peptide measurement in heart failure
2. 筋萎縮性側索硬化症の疫学および病因 epidemiology and pathogenesis of amyotrophic lateral sclerosis
3. 透析患者における赤血球造血刺激因子製剤に対する非鉄薬理学的補助 non iron pharmacologic adjuvants to erythropoiesis stimulating agent therapy in dialysis patients
4. アミロイド心筋症の臨床症状および診断 clinical manifestations and diagnosis of amyloid cardiomyopathy
5. 腎不全における炎症 inflammation in renal insufficiency

English Journal

Uptake and toxicity of copper oxide nanoparticles in cultured primary brain astrocytes.

Bulcke F1, Thiel K, Dringen R.Author information 1Center for Biomolecular Interactions Bremen, University of Bremen , Bremen , Germany.AbstractTo test for consequences of an exposure of brain cells to copper oxide nanoparticles (CuO-NPs), we synthesised and characterised dimercaptosuccinate-coated CuO-NPs. These particles had a diameter of around 5 nm as determined by transmission electron microscopy, while their average hydrodynamic diameter in aqueous dispersion was 136 ± 4 nm. Dispersion in cell-culture medium containing 10% fetal calf serum increased the hydrodynamic diameter to 178 ± 12 nm and shifted the zeta potential of the particles from -49 ± 7 mV (in water) to -10 ± 3 mV. Exposure of cultured primary brain astrocytes to CuO-NPs increased the cellular copper levels and compromised the cell viability in a time-, concentration- and temperature-dependent manner. Application of CuO-NPs in concentrations above 100 µM copper (6.4 µg/ml) severely compromised the viability of the cells, as demonstrated by a lowered 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction capacity, a lowered cellular lactate dehydrogenase activity and an increased membrane permeability for the fluorescent dye propidium iodide. Copper internalisation as well as cell toxicity of astrocytes exposed to CuO-NPs were similar to that observed for cells that had been incubated with copper salts. The CuO-NP-induced toxicity was accompanied by an increase in the generation of reactive oxygen species (ROS) in the cells. Both, ROS formation and cell toxicity in CuO-NP-treated astrocytes, were lowered in the presence of the cell-permeable copper chelator tetrathiomolybdate. These data demonstrate that CuO-NPs are taken up by cultured astrocytes and suggest that excess of internalised CuO-NPs cause cell toxicity by accelerating the formation of ROS.
Nanotoxicology.Nanotoxicology.2014 Nov;8(7):775-85. doi: 10.3109/17435390.2013.829591. Epub 2013 Aug 22.
To test for consequences of an exposure of brain cells to copper oxide nanoparticles (CuO-NPs), we synthesised and characterised dimercaptosuccinate-coated CuO-NPs. These particles had a diameter of around 5 nm as determined by transmission electron microscopy, while their average hydrodynamic diame
PMID 23889294

Histopathology of fathead minnow (Pimephales promelas) exposed to hydroxylated fullerenes.

Jovanović B1, Whitley EM, Palić D.Author information 1Chair for Fish Diseases and Fisheries Biology, Faculty of Veterinary Medicine, Ludwig Maximilians University of Munich (LMU) , Munich , Germany.AbstractHydroxylated fullerenes are reported to be very strong antioxidants, acting to quench reactive oxygen species, thus having strong potential for important and widespread applications in innovative therapies for a variety of disease processes. However, their potential for toxicological side effects is still largely controversial and unknown. Effects of hydroxylated fullerenes C60(OH)24 on the fathead minnow (Pimephales promelas) were investigated microscopically after a 72-hour (acute) exposure by intraperitoneal injection of 20 ppm of hydroxylated fullerenes per gram of body mass. Cumulative, semi-quantitative histopathologic evaluation of brain, liver, anterior kidney, posterior kidney, skin, coelom, gills and the vestibuloauditory system revealed significant differences between control and hydroxylated fullerene-treated fish. Fullerene-treated fish had much higher cumulative histopathology scores. Histopathologic changes included loss of cellularity in the interstitium of the kidney, a primary site of haematopoiesis in fish, and loss of intracytoplasmic glycogen in liver. In the coelom, variable numbers of leukocytes, including many macrophages and fewer heterophils and rodlet cells, were admixed with the nanomaterial. These findings raise concern about in vivo administration of hydroxylated fullerenes in experimental drugs and procedures in human medicine, and should be investigated in more detail.
Nanotoxicology.Nanotoxicology.2014 Nov;8(7):755-63. doi: 10.3109/17435390.2013.828794. Epub 2013 Aug 22.
Hydroxylated fullerenes are reported to be very strong antioxidants, acting to quench reactive oxygen species, thus having strong potential for important and widespread applications in innovative therapies for a variety of disease processes. However, their potential for toxicological side effects is
PMID 23883179

The European Medicines Agency approval of 5-aminolaevulinic acid (Ameluz) for the treatment of actinic keratosis of mild to moderate intensity on the face and scalp: summary of the scientific assessment of the Committee for Medicinal Products for Human Use.

Tzogani K1, Straube M, Hoppe U, Kiely P, O'Dea G, Enzmann H, Salmon P, Salmonson T, Pignatti F.Author information 1European Medicines Agency , London.AbstractThe European Commission has recently issued a marketing authorisation valid throughout the European Union for 5-aminolaevulinic acid (Ameluz). The decision was based on the favorable opinion of the CHMP recommending a marketing authorization for 5-aminolaevulinic acid for treatment of actinic keratosis of mild to moderate intensity on the face and scalp. The active substance is a sensitizer used in photodynamic/radiation therapy (ATC code L01XD04). The gel should cover the lesions and approximately 5 mm of the surrounding area with a film of about 1 mm thickness. The entire treatment area should be illuminated with a red light source, either with a narrow spectrum around 630 nm and a light dose of approximately 37 J/cm(2) or a broader and continuous spectrum in the range between 570 and 670 nm with a light dose between 75 and 200 J/cm(2). One session of photodynamic therapy should be administered for single or multiple lesions. Non- or partially responding lesions should be retreated in a second session 3 months after the first treatment. 5-aminolaevulinic acid is metabolized to protoporphyrin IX, a photoactive compound which accumulates intracellularly in the treated actinic keratosis lesions. Protoporphyrin IX is activated by illumination with red light of a suitable wavelength and energy. In the presence of oxygen, reactive oxygen species are formed which causes damage of cellular components and eventually destroys the target cells. The benefit with 5-aminolaevulinic acid is its ability to improve the complete response rate of actinic keratosis lesions. The most common side effects are reactions at the site of application. The objective of this article is to summarize the scientific review of the application. The detailed scientific assessment report and product information, including the summary of product characteristics (SmPC), are available on the EMA website (www.ema.europa.eu).
The Journal of dermatological treatment.J Dermatolog Treat.2014 Oct;25(5):371-4. doi: 10.3109/09546634.2013.789474. Epub 2013 May 21.
The European Commission has recently issued a marketing authorisation valid throughout the European Union for 5-aminolaevulinic acid (Ameluz). The decision was based on the favorable opinion of the CHMP recommending a marketing authorization for 5-aminolaevulinic acid for treatment of actinic kerato
PMID 23550714

Japanese Journal

Stabilization of Emulsion and Butter like Products Containing Essential Fatty Acids Using Kalonji Seeds Extract and Curcuminoids

Rege Sameera A.,Momin Shamim A.,Bhowmick Dipti N.,Pratap Amit A.
Journal of Oleo Science 61(1), 11-16, 2012
… In RSFO, though curcuminoids alone exerted pro-oxidant effect, KEE and curcuminoids showed synergistic antioxidant activity that was comparable to TBHQ. …
NAID 130001882200

Effects of Sulfaphenazole after Collagenase-Induced Experimental Intracerebral Hemorrhage in Rats

Hama Sayuri,Ishihara Yasuhiro,Watanabe Masatomo,Danjo Sonoko,Nakamura Yu,Itoh Kouichi
Biological and Pharmaceutical Bulletin 35(10), 1849-1853, 2012
… The free-radical hypothesis for intracerebral hemorrhage is based on the cytotoxicity triggered by blood components and its degradation products, such as heme and iron as a potent pro-oxidant atom. …
NAID 130001872384

Oxidative Stress and Mitochondrial Dysfunction in Neurovascular Injury after Stroke(<SPECIAL ISSUE>Neuroscience for the Development of Neurosurgery in the Near Futre)