engleski

Sustituted guanidine compounds as inhibitors of nonenzymatic glycation in vitro

Pathologic effects of the process of nonenzymatic glycation reflect in degenerative changes during ageing, chronic complications of diabetes mellitus and renal failure, and have also been recognised in some neurologic diseases such as Alzheimer's disease. Aminoguanidine has been extensively studied as an inhibitor of nonenzymatic glycation, both in vitro and in vivo. We investigated the inhibiting potency of substituted guanidines in the process of glycation. For this purpose, ƒŃ-methylguanidine-acetic acid (creatine) and dimethylbiguanide (Metformin) were chosen. A common feature of these compounds is the presence of guanidine group in the molecule. Creatine is a specific muscle tissue metabolite, a non-toxic biogenic substance. Dimethylbiguanide is a substituted molecule of guanidine structure, in clinical practice used in the treatment of non-insulin dependent type of diabetes mellitus. Both agents, ƒŃ-methylguanidine-acetic acid and dimethylbiguanide, tested at concentrations of 2.5, 5, 10 and 20 mmol/l, showed a concentration dependent inhibition of the glucose induced albumin glycation in vitro. The inhibiting effect of substituted guanidines was somewhat inferior (17%) to the effect of aminoguanidine inhibition (52%); however, the former substances are valuable for being safe for human use.

nonenzymatic glycation; inhibition; creatine; dimethylbiguanide

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