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  • 1
    Electronic Resource
    Electronic Resource
    Aminoguanidine does not inhibit the initial phase of experimental diabetic retinopathy in rats (1995)
    Springer
    Diabetologia 38 (1995), S. 269-273 
    Details
    ISSN: 1432-0428
    Keywords: Key words Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; retinal basement membrane.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have previously shown that long-term administration of aminoguanidine, an inhibitor of advanced glycosylation product formation, reduces the extent of experimental diabetic retinopathy in the rat by 85 %. In order to determine whether the residual retinopathy that developed despite aminoguanidine was attributable to advanced glycation endproduct formation, a time-course study was performed in three different groups of male Wistar rats: non-diabetic controls (NC), streptozotocin-diabetic controls (DC) and streptozotocin-diabetic rats treated with aminoguanidine HCL, 50 mg/100 ml drinking water (D-AG). Eyes were obtained at 24, 32, 44 and 56 weeks of diabetes/treatment duration and morphologic evaluation was done on retinal digest preparations. At 56 weeks, retinal basement membrane thickness was additionally measured. After 24 weeks of diabetes, the number of acellular capillaries was significantly elevated in DC (44.6 ± 5.7/mm2 of retinal area, NC 19.6 ± 4.9; p 〈 0.001) and increased continuously over time (DC 56 weeks 87.4 ± 15.1; p 〈 0.001 vs DC 24 weeks). In contrast, acellular capillaries in D-AG increased over the first 24 weeks and then remained constant for the rest of the study (D-AG 24 weeks 35.7 ± 5.18; p 〈 0.01 vs NC 24 weeks and NS vs DC 24 weeks; D-AG 56 weeks 42.0 ± 6.20; p NS vs D-AG 24 weeks). Diabetes-associated pericyte loss (DC 24 weeks 2310 ± 170/mm2 of capillary area; NC 24 weeks 3120 ± 190; p 〈 0.001; DC 56 weeks 1570 ± 230; NC 56 weeks 2960 ± 50; p 〈 0.001) was significantly prevented by aminoguanidine after diabetic-like changes over the initial 24 weeks (D-AG 24 weeks 2450 ± 75; p NS vs DC 24 weeks; D-AG 56 weeks 2350 ± 90; p 〈 0.001 vs DC 56 weeks). At 56 weeks, aminoguanidine treatment was associated with a 67.4 % reduction in retinal basement membrane thickening. This time-course study demonstrates that aminoguanidine prevents the progression of experimental diabetic retinopathy, and suggests that non AG-inhibitable mechanisms are involved in the initial phase of diabetic retinopathy. [Diabetologia (1995) 38: 269–273]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400629
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Aminoguanidine does not inhibit the initial phase of experimental diabetic retinopathy in rats (1995)
    Springer
    Diabetologia 38 (1995), S. 269-273 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; retinal basement membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have previously shown that long-term administration of aminoguanidine, an inhibitor of advanced glycosylation product formation, reduces the extent of experimental diabetic retinopathy in the rat by 85%. In order to determine whether the residual retinopathy that developed despite aminoguanidine was attributable to advanced glycation endproduct formation, a time-course study was performed in three different groups of male Wistar rats: non-diabetic controls (NC), streptozotocin-diabetic controls (DC) and streptozotocin-diabetic rats treated with aminoguanidine HCL, 50 mg/100 ml drinking water (D-AG). Eyes were obtained at 24, 32, 44 and 56 weeks of diabetes/treatment duration and morphologic evaluation was done on retinal digest preparations. At 56 weeks, retinal basement membrane thickness was additionally measured. After 24 weeks of diabetes, the number of acellular capillaries was significantly elevated in DC (44.6±5.7/mm2 of retinal area, NC 19.6±4.9; p〈0.001) and increased continuously over time (DC 56 weeks 87.4±15.1; p〈0.001 vs DC 24 weeks). In contrast, acellular capillaries in D-AG increased over the first 24 weeks and then remained constant for the rest of the study (D-AG 24 weeks 35.7±5.18; p〈0.01 vs NC 24 weeks and NS vs DC 24 weeks; D-AG 56 weeks 42.0±6.20; p NS vs D-AG 24 weeks). Diabetes-associated pericyte loss (DC 24 weeks 2310±170/mm2 of capillary area; NC 24 weeks 3120±190; p〈0.001; DC 56 weeks 1570±230; NC 56 weeks 2960±50; p〈0.001) was significantly prevented by aminoguanidine after diabetic-like changes over the initial 24 weeks (D-AG 24 weeks 2450±75; p NS vs DC 24 weeks; D-AG 56 weeks 2350±90; p〈0.001 vs DC 56 weeks). At 56 weeks, aminoguanidine treatment was associated with a 67.4% reduction in retinal basement membrane thickening. This time-course study demonstrates that aminoguanidine prevents the progression of experimental diabetic retinopathy, and suggests that non AG-inhibitable mechanisms are involved in the initial phase of diabetic retinopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400629
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Inhibition of ζ-crystallin by coumarins: A structure-activity study (1996)
    Springer
    The protein journal 15 (1996), S. 261-264 
    Details
    ISSN: 1573-4943
    Keywords: Coumarins ; lens ; NADPH:quinone oxidoreductase ; ζ-crystallin ; inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract A structure-activity study was carried out to determine the important groups of coumarin derivatives in inhibiting the oxidoreductase activity of the camel lensζ-crystallin. Coumarin, 4-hydroxycoumarin, 7-hydroxy-4-methylcoumarin, dicoumarol, and warfarin were screened for their inhibitory effect onζ-crystallin activity. The sequence of potency for the inhibitors was dicoumarol 〉 4-hydroxycoumarin 〉 warfarin ≫ coumarin. 7-Hydroxy-4-methylcoumarin was ineffective as an inhibitor. Only dicoumarol, 4-hydroxycoumarin, and warfarin were found to inhibit the oxidoreductase activity in micromolar ranges. All tested inhibitors seem to act in reversible and time-independent manner. Concentration causing 50% inhibition of the enzyme activity (IC 50 value) was 34μM for dicoumarol, 76μM for 4-hydroxycoumarin, and approximately 515μM for warfarin, while 1 mM coumarin showed less than 10% inhibition. Kinetic analysis revealed inhibition of camel lensζ-crystallin by coumarin derivatives to occur in a competitive manner with respect to dichlorophenolindophenol (DCIP) as an electron acceptor and uncompetitive manner with respect to NADPH as an electron donor. TheK i values were found to be 16μM for dicoumarol, 40μM for 4-hydroxycoumarin, and 220μM for warfarin. The structure-activity relationship of coumarin derivatives indicates that the phenolic hydroxyl group at the C-4 position in the coumarin skeleton is important for the maximal inhibition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01887114
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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