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-inflammatory drugs, Chem. Biol. Drug Des. 73 (2009) 328--338; DOI: 10.1111/j.1747-0285.2009.00774.x. Z. Rajić, I. Perković, I. Butula, B. Zorc, D. Hadjipavlou-Litina, E. Pontiki, S. Pepeljnjak and I. Kosalec, Synthesis and biological evaluation of O -methyl and O -ethyl NSAID hydroxamic acids, J. Enz. Inhib. Med. Chem. 24 (2009), in press. H. E. Miller, Simplified method for the evaluation of antioxidants, J. Am. Oil Chem. Soc. 48 (1971) 91; DOI: 10.1007/BF02635693. M. S. Al-Saikhan, L. R. Howard and J. C. Miller Jr., Antioxidant activity and total phenolics in different

, Z. Rajić, B. Zorc, M. Kralj, M. Marjanović, K. Pavelić, E. De Clercq, G. Andrei, R. Snoeck, J. Balzarini and M. Mintas, The novel phosphoramidate prodrugs of NSAID 3-hydroxypropylamides: Synthesis, cytostatic and antiviral activity evaluations, Eur. J. Med. Chem. 44 (2009) 143-151; DOI: 10.1016/j.ejmech.2008.03.037. 9. I. Perković, I. Butula, M. Kralj, I. Martin-Kleiner, J. Balzarini, D. Hadjipavlou-Litina, A-M. Katsori and B. Zorc, Novel NSAID 1-acyl-4-cycloalkyl/arylsemicarbazides and 1-acyl-5-benzyloxy/ hydroxy)carbamoylcarbazides as potential anticancer

-schizontocidal antimalarial activities of 2-substituted/2,5-disubstituted-8-quinolinamines and some of their amino acid conjugates, Bioorg. Med. Chem.   12 (2004) 1003-1010; DOI: 10.1016/j.bmc.2003.12.029. M. Šimunović, I. Perković, B. Zorc, K. Ester, M. Kralj, D. Hadjipavlou-Litina and E. Pontiki, Urea and carbamate derivatives of primaquine: Synthesis, cytostatic and antioxidant activities, Bioorg. Med. Chem.   17 (2009) 5605-5613; DOI: 10.1016/j.bmc.2009.06.030. M. Zovko Končić, Z. Rajić, N. Petrić and B. Zorc, Antioxidant activity of NSAID hydroxamic acids, Acta Pharm.   59 (2009

angiogenesis by NSAIDs: molecular mechanisms and clinical implications, J. Mol. Med., 2003, 81, 627–636 http://dx.doi.org/10.1007/s00109-003-0479-y [46] Dormond O., Foletti A., Paroz C., Ruegg C., NSAIDs inhibit alpha V beta 3 integrin-mediated and Cdc42/Rac-dependent endothelial-cell spreading, migration and angiogenesis, Nat. Med., 2001, 7, 1041–1047 http://dx.doi.org/10.1038/nm0901-1041 [47] Szabo I.L., Pai R., Soreghan B., Jones M.K., Baatar D., Kawanaka H., et al., NSAIDs inhibit the activation of egr-1 gene in microvascular endothelial cells. A key to inhibition of

. 1998;19(4):141–7. 27. Beiche F, Scheuerer S, Brune K, Geisslinger G, Goppelt-Struebe M. Up-regulation of cyclo-oxygenase-2 mRNA in the rat spinal cord following peripheral inflammation. FEBS Lett. 1996;390(2):165–9. 28. Mitchell JA, Warner TD. Cyclo-oxygenase-2: pharmacology, physiology, biochemistry and relevance to NSAID therapy. Br J Pharmacol. 1999;128(6):1121-32. DOI: 10.1038/sj.bjp.0702897. 29. Martin WR. General problems of drug abuse and drug dependence. In: Martin WR (eds). Drug Addiction I. Handbuch der experimentellen Pharmakologie / Handbook of

affected by GBM [ 5 ], [ 6 ]. On the other hand, epidemiologic, clinical and experimental reports indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) could be useful drugs endowed with potential anticancer activity [ 7 ], [ 8 ], [ 9 ], [ 10 ]. Previous reports revealed that NSAIDs suppressed tumor growth and malignant transformation through processes such as inhibition of growth or induction of apoptosis and suppression of angiogenesis [ 11 ]. NSAIDs showed their anti-inflammatory activity by suppressing cyclooxygenase (COX) involved in prostaglandin synthesis

ISSN 1203-8407 © 2009 Science & Technology Network, Inc. J. Adv. Oxid. Technol. Vol. 12, No. 2, 2009 164 Comparison of Emerging NSAID Pollutants Degradation in Aqueous Media by O3/UV-VIS Processes Alessandra Coelho1, 2, Fabiola Méndez-Arriaga1, Carmen Sans1, Márcia Dezotti2, Santiago Esplugas*, 1, and Jaime Giménez1 1Department of Chemical Engineering, University of Barcelona, Martí i Franquès 1, 08028, Barcelona, Spain 2Chemical Engineering Program – COPPE – Federal University of Rio de Janeiro, P.O. Box 68502, CEP 21941- 972 Rio de Janeiro, Brazil Abstract

affinity for binding to muscarinic receptors, histaminergic receptors, and noradrenaline transporter [ 12 ]. Fluvoxamine suppresses NSAID (nonsteroidal anti-inflammatory drug)-induced gastric ulcer by increasing the total glutathione and nitric oxide levels. Moreover, fluvoxamine reduces the increase of oxidant parameter level in indomethacin-induced gastric ulcer [ 13 ]. However, to date, there is no study that directly compares the effect of fluvoxamine on stress- and NSAID-induced gastric ulcer. Moreover, there is lack of evidence in the gastroprotective mechanism of

oxidative stress? Circulation 2001;104:1571-4. Schiffrin EL, Park JB, Intengan HD, Touyz RM. Correcton of arterial structure and endothelial dysfunction in human essential hypertension by the angiotensin receptor antagonist losartan. Circulation 2000;101:1653-9. Halperin ML, Kamel KS. Potassium. Lancet 1998;352:135-40. Galešić K, Morović-Vergles J, Jelaković B. Nesteroidni antireumatici i bubreg [Nonsteroidal antirheumatics and the kidney, in Croatian]. Reumatizam 2005;52:61-6. Perazella AM. NSAIDs and the kidney: acute renal failure. In: Lerma VE, Berns SJ, Nissenson AR

unfavourably with the local anaesthetics. 4 Renal failure due to the NSAID in the LIA-solution can occur in elderly frail patients The LIA-technique traditionally requires adrenaline and ketorolac, a potent, water-soluble NSAID, in addition to a local anaesthetic. Fatin Affas in her PhD-studies found that the plasma-concentration of ketorolac was similar to that after the same dose of ketorolac given intramuscularly [ 4 ]. This means that the ketorolac administered via LIA also will have the same negative effects on kidneys as is typical for NSAIDs. Elderly patients should