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Volumn 50, Issue 10, 2011, Pages 2392-2396

Erratum: Acyloxybutadiene-iron tricarbonyl complexes as enzyme-triggered CO-releasing molecules (ET-CORMs) (Angewandte Chemie - International Edition (2011) 50 (2392-2396) DOI 10.1002/anie.201006598);Acyloxybutadiene iron tricarbonyl complexes as enzyme-triggered CO-releasing molecules (ET-CORMs)

Author keywords

Carbonyl ligands; CO release; Drug delivery; Enzyme catalysis; Inhibitors; carbonyl ligands; drug delivery; enzyme catalysis; inhibitors

Indexed keywords

CONTROLLED DRUG DELIVERY; CORROSION INHIBITORS; DRUG DELIVERY; ENZYMES; MOLECULES; NITRIC OXIDE; TARGETED DRUG DELIVERY;

EID: 79952053626     PISSN: 14337851     EISSN: 15213773     Source Type: Journal    
DOI: 10.1002/anie.201190036     Document Type: Erratum
Times cited : (168)

References (40)
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    • note
    • Cyclohexenone-derived complexes may also be considered as meaningful models for the future investigation of related complexes of nontoxic natural products containing a cyclohexenone substructure.
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    • For the enzymatic kinetic resolution of alkoxycarbonyl-substituted diene-iron tricarbonyl complexes, see
    • For the enzymatic kinetic resolution of alkoxycarbonyl-substituted diene-iron tricarbonyl complexes, see: N. W. Alcock, D. H. G. Crout, C. M. Henderson, S. E. Thomas, J. Chem. Soc. Chem. Commun. 1988, 746-747.
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    • note
    • In a control experiment, it was confirmed that compound rac-14 did not show CO release under the conditions of the myoglobin assay in the presence of PLE or LCR.
  • 29
    • 79952058105 scopus 로고    scopus 로고
    • note
    • II form of Mb). Under the assay conditions, typical times for the release of 0.5 mol of CO per mol of ET-CORM are as follows: 56 min for rac-8 (0.09 equiv of LCR), 183 min for rac-12 (0.01 equiv of PLE) and 86 min for rac-13 (0.01 equiv of PLE). Owing to the complexity of the parameter space, such values do not allow a quantitative comparison of the ET-CORMS or any predictions of their biological performance.
  • 32
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    • note
    • Exceptionally high NO quantities account for cell damage, which is a crucial factor in the pathophysiology of human diseases. The gene transcription of iNOS can be induced for example, by lipopolysaccharide (LPS), interferon-γ (IFN-γ), oxidative stress/reactive oxygen species (ROS), interleukin-1β (IL-1β) or tumor necrosis factor-α (TNF-α). This occurs via an activation of nuclear factor-κB (NF-κB). The activation of NF-κB can be prohibited for example by glucocorticosteroids, antioxidants or transforming growth factor-1β (TGF-β1).
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    • note
    • Cytotoxicity is an important issue when dealing with CO-releasing molecules. The toxicity of CO, which leads to its deadly effect in mammals, is due to its high affinity to the prosthetic heme groups of hemoglobin and myoglobin, resulting in hypoxia, together with binding of CO to cytochrome c oxidase in mitochondria. Thus, the mitochondrial electron transport chain is inhibited and a breakdown of the energy supply of the cells is caused.
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    • note
    • This assay is based upon the conversion of the yellow MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) by mitochondrial dehydrogenases into a violet formazan dye, which can be quantified photometrically.
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    • Supernatants of cells were mixed 1:1 (v/v) with Griess reagent (1% sulfanilamide, 0.1% naphthylethylenediamine dihydrochloride in 2% phosphoric acid) and the absorbance was measured at 560 nm. Nitrite content was quantified by using sodium nitrite as standard. See
    • Supernatants of cells were mixed 1:1 (v/v) with Griess reagent (1% sulfanilamide, 0.1% naphthylethylenediamine dihydrochloride in 2% phosphoric acid) and the absorbance was measured at 560 nm. Nitrite content was quantified by using sodium nitrite as standard. See: E. Park, M. R. Quinn, J. Leukocyte Biol. 1993, 54, 119-124.
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    • Park, E.1    Quinn, M.R.2
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    • The ether rac-14 showed a significant iNOS inhibition of (11 ∓ 3)% at a concentration of 100 μM. This effect most likely results from some esterase-independent decomposition reaction.
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    • Potential effects of iron that could act on the transcriptional level of iNOS have not yet been addressed and will be included in further studies. It was shown that free cellular iron can lead to a decrease in iNOS protein expression by an inhibition of gene transcription of iNOS; see
    • Potential effects of iron that could act on the transcriptional level of iNOS have not yet been addressed and will be included in further studies. It was shown that free cellular iron can lead to a decrease in iNOS protein expression by an inhibition of gene transcription of iNOS; see: G. Weiss, G. Werner-Felmayer, E. R. Werner, K. Grünewald, H. Wachter, M. W. Hentze, J. Exp. Med. 1994, 180, 969-976.
    • (1994) J. Exp. Med. , vol.180 , pp. 969-976
    • Weiss, G.1    Werner-Felmayer, G.2    Werner, E.R.3    Grünewald, K.4    Wachter, H.5    Hentze, M.W.6


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.