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George Psomas - One of the best experts on this subject based on the ideXlab platform.
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zn ii complexes of e 4 2 pyridin 2 ylmethylene hydrazinyl quinazoline in combination with non steroidal anti inflammatory Drug sodium diclofenac structure dna binding and photo cleavage studies antioxidant activity and interaction with albumin
Journal of Inorganic Biochemistry, 2020Co-Authors: Chrisoula Kakoulidou, Antonios G Hatzidimitriou, Panagiotis S Gritzapis, Konstantina C Fylaktakidou, George PsomasAbstract:The interaction of the novel quinazoline (E)-4-(2-(pyridin-2-ylmethylene)hydrazinyl)quinazoline (L) with Zn2+ was performed in the absence or presence of the Non-Steroidal Anti-Inflammatory Drug sodium diclofenac (Nadicl) and resulted in the formation of complexes [Zn(L)2](NO3)2·MeOH (1·MeOH) and [Zn(L)(dicl-O)2]·MeOH (2·MeOH), respectively. The two complexes were characterized by IR and 1H NMR spectroscopy and by single-crystal X-ray crystallography. In these complexes, L was tridentately coordinated to Zn(II) via the quinazoline, hydrazone and pyridine nitrogen atoms. Further studies concerning the behavior of the compounds towards calf-thymus (CT) DNA and supercoiled circular pBluescript KS II plasmid DNA (pDNA) have been performed. The complexes may bind to CT DNA via intercalation, with complex 1 showing higher binding affinity than 2. The complexes may cleave pDNA in the absence or presence of irradiation with UVA, UVB or visible light and the most active pDNA-cleavager is compound 1. The binding constants of the compounds for bovine serum albumin were calculated and the subdomain of the albumin where the compounds prefer to bind was determined. The free radical scavenging ability of the compounds was evaluated towards 1,1-diphenyl-picrylhydrazyl and 2,2΄-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) radicals with complex 2 being the most active compound. Thus, complex of type 1 maybe a lead compound for the development of novel DNA-binders and DNA-cleavers or photo-cleavers for medical and biotechnological "on demand" applications, whereas the structure of complex type 2 may provide novel antioxidants and radical scavengers.
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nickel ii complexes of the non steroidal anti inflammatory Drug tolfenamic acid synthesis structure antioxidant activity and interaction with albumins and calf thymus dna
Polyhedron, 2016Co-Authors: Xanthippi Totta, Athanasios N Papadopoulos, Antonios G Hatzidimitriou, George PsomasAbstract:Abstract The reaction of NiCl2·6H2O with the Non-Steroidal Anti-Inflammatory Drug tolfenamic acid (Htolf) in the absence or presence of a nitrogen-donor heterocyclic ligand such as 2,2′-bipyridine (bipy), 1,10-phenanthroline (phen), 2,2′-bipyridylamine (bipyam), 2,2′-dipyridylketone oxime (Hpko) and pyridine (py) led to the formation of six novel Ni(II) mononuclear complexes. The complexes were characterized by physicochemical and spectroscopic techniques and the crystal structures of complexes [Ni(tolf-O)2(bipy)(MeOH)2], 2 and [Ni(tolf-O)2(Hpko-N,N′)2], 5 were determined by X-ray crystallography. The in vitro investigation of the ability of the complexes to scavenge 1,1-diphenyl-picrylhydrazyl, 2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) and hydroxyl radicals and to inhibit soybean lipoxygenase revealed their potential antioxidant activity. The interaction of the complexes to calf-thymus DNA was monitored by diverse techniques (UV spectroscopy, cyclic voltammetry, viscosity measurements) revealing intercalation as the most possible mode of binding. Competitive studies of the complexes with ethidium bromide were monitored by fluorescence emission spectroscopy. The interaction of the complexes with serum albumins was studied by fluorescence emission spectroscopy and the binding constants of the compounds to the albumins were calculated.
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antioxidant capacity and dna interaction studies of zinc complexes with a non steroidal anti inflammatory Drug mefenamic acid
Journal of Inorganic Biochemistry, 2013Co-Authors: Alketa Tarushi, Iztok Turel, George Psomas, Athanasios N Papadopoulos, Zoi Karaflou, Jakob Kljun, Dimitris P KessissoglouAbstract:Zinc(II) complexes of a Non-Steroidal Anti-Inflammatory Drug, mefenamic acid(= Hmef) in the absence or presence of the nitrogen donor heterocyclic ligands 2,2′-bipyridine(= bipy), 2,2′-bipyridylamine(= bipyam), 2,2′-dipyridylketone oxime(= Hpko) or 1,10-phenanthroline(= phen) have been synthesized and characterized. The crystal structures of [Zn(mef-O,O′)2(bipy)], 2, [Zn(mef-O)2(Hpko-N,N′)2]·EtOH, 4 and [Zn(mef-O)(mef-O,O′)(phen)(H2O)], 5, have been determined by X-ray crystallography showing distinct binding modes of mefenamato carboxylato group, bidentate in 2, monodentate in 4 or both in 5. Interaction studies of the complexes with calf-thymus DNA (CT DNA) have shown that complexes can bind to CT DNA with [Zn(mef-O)2(Hpko)2] exhibiting the highest binding constant to CT DNA (Kb = 1.93(± 0.04) × 107 M− 1). The complexes can bind to CT DNA via intercalation as concluded by DNA solution viscosity measurements. Competitive studies with ethidium bromide (EB) have shown that the complexes can displace the DNA-bound EB. The complexes exhibit good binding affinity to serum albumin proteins with [Zn(mef-O)2(H2O)4], 1 exhibiting the highest quenching ability (kq = 1.46 × 1015 M− 1 s− 1 for human and 5.55 × 1015 M− 1 s− 1 for bovine serum albumin). All compounds have been tested for their antioxidant and free radical scavenging activity as well as for their in vitro inhibitory activity against soybean lipoxygenase. The scavenging activity is low to moderate against 1,1-diphenyl-picrylhydrazyl (DPPH) radicals and high against hydroxyl and 2,2′-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS+) radicals, with [Zn(mef-O)2(H2O)4], 1 (ABTS%, 0.1 mM: 94.75(± 1.06)%; OH%, 0.1 mM: 96.69(± 0.27)%; LOX: IC50 = 27.34(± 0.90) μM) exhibiting the highest scavenging activity of the ABTS radical cation among the complexes. Additionally, the complexes exhibit higher scavenging and LOX inhibitory activity than free mefenamic acid (ABTS%, 0.1 mM: 66.32(± 0.38)%; OH%,0.1 mM: 92.51(± 0.44)%; LOX: IC50 = 48.52(± 0.88) μM).
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ni ii complexes with non steroidal anti inflammatory Drug diclofenac structure and interaction with dna and albumins
Polyhedron, 2013Co-Authors: Myrto Kyropoulou, Catherine P Raptopoulou, Vassilis Psycharis, George PsomasAbstract:Abstract The interaction of nickel(II) with the Non-Steroidal Anti-Inflammatory Drug sodium diclofenac (Nadicl) in the presence of the N,N′-donor heterocyclic ligands 2,2′-dipyridylketone oxime (Hpko), 2,2′-bipyridine (bipy) or 1,10-phenanthroline (phen) leads to the formation of mononuclear Ni(II) complexes. The crystal structure of [Ni(dicl)(Hdicl)(Hpko) 2 ](dicl)·CH 3 OH·0.6H 2 O ( 1 ·CH 3 OH·0.6H 2 O) has been determined by X-ray crystallography. The interaction of the complexes with human or bovine serum albumins has been studied by fluorescence spectroscopy revealing their good binding affinity to the albumins with high binding constant values. UV study of the interaction of the complexes with calf-thymus DNA (CT DNA) has shown that the complexes can bind to CT DNA with [Ni(dicl)(Hdicl)(Hpko) 2 ](dicl) exhibiting the highest binding constant to CT DNA. Complex 1 can bind to CT DNA via intercalation as concluded by studying its cyclic voltammograms in the presence of CT DNA solution and by DNA solution viscosity measurements, while for complexes [Ni(dicl) 2 (bipy)] ( 2 ) and [Ni(dicl) 2 (phen)] ( 3 ) a non-classic intercalative mode has been concluded. Competitive studies of the complexes with ethidium bromide (EB) have shown their moderate to significant ability to displace the DNA-bound EB suggesting a competition with EB.
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biological evaluation of cobalt ii complexes with non steroidal anti inflammatory Drug naproxen
Journal of Inorganic Biochemistry, 2012Co-Authors: Filitsa Dimiza, Dimitris P Kessissoglou, Athanasios N Papadopoulos, Vassilis Tangoulis, Vassilis Psycharis, Catherine P Raptopoulou, George PsomasAbstract:Abstract Cobalt(II) complexes with the Non-Steroidal Anti-Inflammatory Drug naproxen in the presence or absence of nitrogen-donor heterocyclic ligands (pyridine, 2,2′-bipyridine or 1,10-phenanthroline) have been synthesized and characterized with physicochemical and spectroscopic techniques. The deprotonated naproxen acts as monodentate ligand coordinated to Co(II) ion through a carboxylato oxygen. The crystal structure of [bis(aqua)bis(naproxenato)bis(pyridine)cobalt(II)], 2 has been determined by X-ray crystallography. The EPR spectrum of complex 2 in frozen solution reveals that it retains its structure. UV study of the interaction of the complexes with calf-thymus DNA (CT DNA) has shown that the complexes can bind to CT DNA and [(2,2′-bipyridine)bis(methanol)bis(naproxenato)cobalt(II)] exhibits the highest binding constant to CT DNA. The cyclic voltammograms of the complexes recorded in DMSO solution and in the presence of CT DNA in 1/2 DMSO/buffer (containing 150 mM NaCl and 15 mM trisodium citrate at pH 7.0) solution have shown that they can bind to CT DNA by the intercalative binding mode which has also been verified by DNA solution viscosity measurements. Competitive study with ethidium bromide (EB) has shown that the complexes can displace the DNA-bound EB indicating that they bind to DNA in strong competition with EB. Naproxen and its cobalt(II) complexes exhibit good binding propensity to human or bovine serum albumin proteins having relatively high binding constant values. The antioxidant activity of the compounds has been evaluated indicating their high scavenging activity against hydroxyl free radicals and superoxide radicals.
Andrew R Moore - One of the best experts on this subject based on the ideXlab platform.
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single dose oral fenoprofen for acute postoperative pain in adults
Cochrane Database of Systematic Reviews, 2011Co-Authors: Mx Traa, Sheena Derry, Andrew R MooreAbstract:Background Fenoprofen is a Non-Steroidal Anti-Inflammatory Drug (NSAID), available in several different countries, but not widely used.
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single dose oral fenbufen for acute postoperative pain in adults
Cochrane Database of Systematic Reviews, 2009Co-Authors: Andrew R Moore, Sheena Derry, Henry J McquayAbstract:Background Fenbufen is a non-selective Non-Steroidal Anti-Inflammatory Drug (NSAID), used to treat acute and chronic painful conditions. There is no known systematic review of its use in acute postoperative pain.
Dimitris P Kessissoglou - One of the best experts on this subject based on the ideXlab platform.
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antioxidant capacity and dna interaction studies of zinc complexes with a non steroidal anti inflammatory Drug mefenamic acid
Journal of Inorganic Biochemistry, 2013Co-Authors: Alketa Tarushi, Iztok Turel, George Psomas, Athanasios N Papadopoulos, Zoi Karaflou, Jakob Kljun, Dimitris P KessissoglouAbstract:Zinc(II) complexes of a Non-Steroidal Anti-Inflammatory Drug, mefenamic acid(= Hmef) in the absence or presence of the nitrogen donor heterocyclic ligands 2,2′-bipyridine(= bipy), 2,2′-bipyridylamine(= bipyam), 2,2′-dipyridylketone oxime(= Hpko) or 1,10-phenanthroline(= phen) have been synthesized and characterized. The crystal structures of [Zn(mef-O,O′)2(bipy)], 2, [Zn(mef-O)2(Hpko-N,N′)2]·EtOH, 4 and [Zn(mef-O)(mef-O,O′)(phen)(H2O)], 5, have been determined by X-ray crystallography showing distinct binding modes of mefenamato carboxylato group, bidentate in 2, monodentate in 4 or both in 5. Interaction studies of the complexes with calf-thymus DNA (CT DNA) have shown that complexes can bind to CT DNA with [Zn(mef-O)2(Hpko)2] exhibiting the highest binding constant to CT DNA (Kb = 1.93(± 0.04) × 107 M− 1). The complexes can bind to CT DNA via intercalation as concluded by DNA solution viscosity measurements. Competitive studies with ethidium bromide (EB) have shown that the complexes can displace the DNA-bound EB. The complexes exhibit good binding affinity to serum albumin proteins with [Zn(mef-O)2(H2O)4], 1 exhibiting the highest quenching ability (kq = 1.46 × 1015 M− 1 s− 1 for human and 5.55 × 1015 M− 1 s− 1 for bovine serum albumin). All compounds have been tested for their antioxidant and free radical scavenging activity as well as for their in vitro inhibitory activity against soybean lipoxygenase. The scavenging activity is low to moderate against 1,1-diphenyl-picrylhydrazyl (DPPH) radicals and high against hydroxyl and 2,2′-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS+) radicals, with [Zn(mef-O)2(H2O)4], 1 (ABTS%, 0.1 mM: 94.75(± 1.06)%; OH%, 0.1 mM: 96.69(± 0.27)%; LOX: IC50 = 27.34(± 0.90) μM) exhibiting the highest scavenging activity of the ABTS radical cation among the complexes. Additionally, the complexes exhibit higher scavenging and LOX inhibitory activity than free mefenamic acid (ABTS%, 0.1 mM: 66.32(± 0.38)%; OH%,0.1 mM: 92.51(± 0.44)%; LOX: IC50 = 48.52(± 0.88) μM).
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biological evaluation of cobalt ii complexes with non steroidal anti inflammatory Drug naproxen
Journal of Inorganic Biochemistry, 2012Co-Authors: Filitsa Dimiza, Dimitris P Kessissoglou, Athanasios N Papadopoulos, Vassilis Tangoulis, Vassilis Psycharis, Catherine P Raptopoulou, George PsomasAbstract:Abstract Cobalt(II) complexes with the Non-Steroidal Anti-Inflammatory Drug naproxen in the presence or absence of nitrogen-donor heterocyclic ligands (pyridine, 2,2′-bipyridine or 1,10-phenanthroline) have been synthesized and characterized with physicochemical and spectroscopic techniques. The deprotonated naproxen acts as monodentate ligand coordinated to Co(II) ion through a carboxylato oxygen. The crystal structure of [bis(aqua)bis(naproxenato)bis(pyridine)cobalt(II)], 2 has been determined by X-ray crystallography. The EPR spectrum of complex 2 in frozen solution reveals that it retains its structure. UV study of the interaction of the complexes with calf-thymus DNA (CT DNA) has shown that the complexes can bind to CT DNA and [(2,2′-bipyridine)bis(methanol)bis(naproxenato)cobalt(II)] exhibits the highest binding constant to CT DNA. The cyclic voltammograms of the complexes recorded in DMSO solution and in the presence of CT DNA in 1/2 DMSO/buffer (containing 150 mM NaCl and 15 mM trisodium citrate at pH 7.0) solution have shown that they can bind to CT DNA by the intercalative binding mode which has also been verified by DNA solution viscosity measurements. Competitive study with ethidium bromide (EB) has shown that the complexes can displace the DNA-bound EB indicating that they bind to DNA in strong competition with EB. Naproxen and its cobalt(II) complexes exhibit good binding propensity to human or bovine serum albumin proteins having relatively high binding constant values. The antioxidant activity of the compounds has been evaluated indicating their high scavenging activity against hydroxyl free radicals and superoxide radicals.
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non steroidal anti inflammatory Drug diflunisal interacting with cu ii structure and biological features
Journal of Inorganic Biochemistry, 2011Co-Authors: Stella Fountoulaki, Franc Perdih, Iztok Turel, Dimitris P Kessissoglou, George PsomasAbstract:Copper(II) complexes with the Non-Steroidal Anti-Inflammatory Drug diflunisal in the presence of N,N-dimethylformamide or nitrogen donor heterocyclic ligands (pyridine, 1,10-phenanthroline, 2,2'-bipyridine or 2,2'-bipyridylamine) have been synthesized and characterized. The deprotonated diflunisal ligands are coordinated to Cu(II) ion through carboxylato oxygen atoms. The crystal structures of [tetrakis(diflunisal)bis(N,N-dimethylformamide)dicopper(II)] 1 and [bis(diflunisal)bis(pyridine)copper(II)], 2 have been determined by X-ray crystallography and are the first reported crystal structures of diflunisal complexes. UV study of the interaction of the complexes with calf-thymus DNA (CT DNA) suggests binding of the complexes to CT DNA with the dinuclear [tetrakis(diflunisal)bis(N,N-dimethylformamide)dicopper(II)] compound exhibiting the highest binding constant, K(b). Intercalative binding mode may also be concluded using cyclic voltammetry and solution viscosity measurements of the complexes in the presence of CT DNA. Competitive studies with ethidium bromide (EB) indicate that the complexes can displace the DNA-bound EB suggesting competition with EB. Diflunisal and its complexes exhibit good binding propensity to human or bovine serum albumin protein showing relatively high binding constant values.
Uday Bandyopadhyay - One of the best experts on this subject based on the ideXlab platform.
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indomethacin a non steroidal anti inflammatory Drug develops gastropathy by inducing reactive oxygen species mediated mitochondrial pathology and associated apoptosis in gastric mucosa a novel role of mitochondrial aconitase oxidation
Journal of Biological Chemistry, 2009Co-Authors: Pallab Maity, Samik Bindu, Athar Alam, Manish Goyal, Kalyan Mitra, Uday BandyopadhyayAbstract:Abstract We have investigated the role of mitochondria on the development of indomethacin (a Non-Steroidal Anti-Inflammatory Drug)-induced gastric mucosal apoptosis and associated gastropathy in rat. Transmission electron microscopic studies indicate that indomethacin damages mitochondrial ultrastructure and causes mitochondrial dysfunction as evident from decreased stage-3 respiration, dehydrogenase activity, and transmembrane potential (ΔΨm). Mitochondrial pathology is associated with increased generation of intra-mitochondrial-reactive oxygen species, such as , H2O2 and ·OH, leading to oxidative stress. is the most effective to damage mitochondrial aconitase, leading to the release of iron from its iron-sulfur cluster. The released iron, by interacting with intra-mitochondrial H2O2, forms ·OH. Immunoprecipitation of mitochondrial aconitase and subsequent Western immunoblotting indicate carbonylation of aconitase along with the loss of activity in vivo after indomethacin treatment. The release of iron has been documented by fluorescence imaging of mucosal cells by using Phen Green SK, a specific probe for chelatable iron. Interestingly, intra-mitochondrial ·OH generation is crucial for the development of mitochondrial pathology and activation of mitochondrial death pathway by indomethacin. Scavenging of ·OH by dimethyl sulfoxide or α-phenyl-n-tert-butylnitrone, a spin-trap, prevents indomethacin-induced mitochondrial ultrastructural changes, oxidative stress, collapse of ΔΨm, and mitochondrial dysfunction. The scavengers also restore indomethacin-induced activation of caspase-9 and caspase-3 to block mitochondrial pathway of apoptosis and gastric mucosal damage. This study, thus, reveals the critical role of -mediated mitochondrial aconitase inactivation to release intra-mitochondrial iron, which by generating ·OH promotes gastric mucosal cell apoptosis and gastropathy during indomethacin treatment.
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indomethacin a non steroidal anti inflammatory Drug develops gastropathy by inducing reactive oxygen species mediated mitochondrial pathology and associated apoptosis in gastric mucosa a novel role of mitochondrial aconitase oxidation
Journal of Biological Chemistry, 2009Co-Authors: Pallab Maity, Chinmay Pal, Samik Bindu, Sumanta Dey, Athar Alam, Manish Goyal, Kalyan Mitra, Uday BandyopadhyayAbstract:We have investigated the role of mitochondria on the development of indomethacin (a Non-Steroidal Anti-Inflammatory Drug)-induced gastric mucosal apoptosis and associated gastropathy in rat. Transmission electron microscopic studies indicate that indomethacin damages mitochondrial ultrastructure and causes mitochondrial dysfunction as evident from decreased stage-3 respiration, dehydrogenase activity, and transmembrane potential (DeltaPsi(m)). Mitochondrial pathology is associated with increased generation of intra-mitochondrial-reactive oxygen species, such as O(2)(*), H(2)O(2) and *OH, leading to oxidative stress. O(2)(*) is the most effective to damage mitochondrial aconitase, leading to the release of iron from its iron-sulfur cluster. The released iron, by interacting with intra-mitochondrial H(2)O(2), forms *OH. Immunoprecipitation of mitochondrial aconitase and subsequent Western immunoblotting indicate carbonylation of aconitase along with the loss of activity in vivo after indomethacin treatment. The release of iron has been documented by fluorescence imaging of mucosal cells by using Phen Green SK, a specific probe for chelatable iron. Interestingly, intra-mitochondrial *OH generation is crucial for the development of mitochondrial pathology and activation of mitochondrial death pathway by indomethacin. Scavenging of *OH by dimethyl sulfoxide or alpha-phenyl-n-tert-butylnitrone, a spin-trap, prevents indomethacin-induced mitochondrial ultrastructural changes, oxidative stress, collapse of DeltaPsi(m), and mitochondrial dysfunction. The scavengers also restore indomethacin-induced activation of caspase-9 and caspase-3 to block mitochondrial pathway of apoptosis and gastric mucosal damage. This study, thus, reveals the critical role of O(2)(*)-mediated mitochondrial aconitase inactivation to release intra-mitochondrial iron, which by generating *OH promotes gastric mucosal cell apoptosis and gastropathy during indomethacin treatment.
Mario Thevis - One of the best experts on this subject based on the ideXlab platform.
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detection of the diuretic hydrochlorothiazide in a doping control urine sample as the result of a non steroidal anti inflammatory Drug nsaid tablet contamination
Forensic Science International, 2016Co-Authors: Hansjorg Helmlin, Andre Murner, Samuel Steiner, Matthias Kamber, Christina Weber, Hans Geyer, Sven Guddat, Wilhelm Schanzer, Mario ThevisAbstract:Abstract Hydrochlorothiazide (HCTZ, 6-chloro-3,4-dihydro-2 H -1,2,4-benzothiadiazine-7-sulfonamide-1,1-dioxide) belongs to the class of diuretic agents that represent one of today's cornerstones of the treatment of hypertensive patients. In addition to its clinical relevance, HCTZ is prohibited in sports according to the regulations of the World Anti-Doping Agency (WADA) at all times and has frequently been detected in sports Drug testing urine samples worldwide since its ban was introduced in 1988. Despite these facts, the adverse analytical finding concerning HCTZ in an in-competition routine doping control sample collected in December 2014 was further investigated, particularly motivated by the comparably low urinary concentration of the Drug accounting for approximately 5ng/mL. The athlete in question did not declare the use of any nutritional supplement or medication other than the ingestion of a Non-Steroidal Anti-Inflammatory Drug (NSAID) prior to competition. Hence, the Drug (formulated as coated tablet) provided by the athlete as well as the corresponding retention sample of the manufacturer were analyzed. Noteworthy, both samples confirmed the presence of about 2μg of HCTZ per tablet. In order to further probe for the plausibility of the observed urinary HCTZ concentrations with the scenario of Drug ingestion and subsequent doping control sample collection, administration studies with produced HCTZ-spiked placebo-tablets (2.5μg of HCTZ/tablet) were conducted. Urine specimens were collected prior to and after ingestion of the Drug and subjected to routine doping control analytical procedures employing liquid chromatography/tandem mass spectrometry. While blank urine samples returned negative test results, post-administration specimens were found to contain HCTZ at concentrations of approximately 1–16ng/mL, which supported the athlete's inadvertent intake of HCTZ via contaminated NSAID tablets. Due to the substantial sensitivity of test methods employed today by doping control laboratories, even Drug contaminations ranging within the good manufacturing practice (GMP) limit of 10ppm overall carry-over can evidently lead to adverse analytical findings. This calls into question whether selected (classes of) substances such as diuretics should be reported only when exceeding a defined reporting level and/or whether adverse analytical findings of non-threshold substances should be reported with an estimated semi-quantitative concentration of the identified substance to facilitate the result management by anti-doping organizations.