Mono- and diaminoguanidine inhibited ambient glucose-induced glycosylated end product formation of albumin and collagen 125I-labeled albumin covalent binding in vitro. Diaminoguanidine was a stronger inhibitor than monoaminoguanidine. These compounds also inhibited rat eye lens aldose reductase activity in vitro noncompetitively with respect to NADPH with Ki = 30.6 mM for monoaminoguanidine and Ki = 12.5 mM for diaminoguanidine. When administered daily for 98 days at a dose of 25 mg/kg body wt i.p., both compounds lowered eye lens sorbitol and aldose reductase activity in normoglycemic and alloxan-induced diabetic rats. Again, diaminoguanidine was a better inhibitor. Daily long-term administration of mono- and diaminoguanidine (25 mg/kg body wt i.p.) inhibited and prevented experimental diabetes–induced lens opacity in rats, respectively. It appears that diaminoguanidine has a better therapeutic potential in controlling diabetic complications.
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Original Articles| August 01 1991
Inhibition of Diabetes-Associated Complications by Nucleophilic Compounds
Address correspondence to Maharaj K. Sahib, Division of Biochemistry, Central Drug Research Institute, Lucknow 226 001, India.
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Kshama Kumari, Shahid Umar, Veena Bansal, Maharaj K Sahib; Inhibition of Diabetes-Associated Complications by Nucleophilic Compounds. Diabetes 1 August 1991; 40 (8): 1079–1084. https://doi.org/10.2337/diab.40.8.1079
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