Abstract
The micro- and macro-complications in diabetes mellitus (DM) mainly arise from the damage induced by Amadori and advanced glycation end products, as well as the released free radicals. The primary goal of DM treatment is to reduce the risk of micro- and macro-complications. In this study, we looked at the efficacy of aminoguanidine (AG) to prevent the production of early glycation products in alloxan-diabetic rabbits. Type1 DM was induced in rabbits by a single intravenous injection of alloxan (90 mg/kg body weight). Another group of rabbits was pre-treated with AG (100 mg/kg body weight) prior to alloxan injection; this was followed by weekly treatment with 100 mg/kg of AG for eight weeks. Glucose, insulin, and early glycation products (HbA1C and fructosamine) were measured in control, diabetic and AG treated diabetic rabbits. The effects of hyperglycemia on superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (Gpx), reduced glutathione (rGSH), nitric oxide, lipid peroxides, and protein carbonyl were investigated. Alloxan-diabetic rabbits had lower levels of SOD, CAT, Gpx, and rGSH than control rabbits. Nitric oxide levels were considerably greater. AG administration restored the activities of SOD, CAT, Gpx enzymes up to 70–80% and ameliorated the nitric oxide production. HbA1c and fructosamine levels were considerably lower in AG-treated diabetic rabbits. The observed control of hyperglycemia and amadori adducts in alloxan-diabetic rabbits by AG may be attributed to decrease of stress and restoration of antioxidant defenses.
Highlights
Hyperglycemia can accelerate non-enzymatic glycation of moving and tissue-fixed proteins, which can lead to secondary problems in diabetes mellitus (DM) [1, 2]
The findings suggested that AG ameliorated Amadori product formation
Chronic hyperglycemia in diabetics may cause extensive non-enzymatic glycation of proteins leading to early- and advanced-glycation end products
Summary
Hyperglycemia can accelerate non-enzymatic glycation of moving and tissue-fixed proteins, which can lead to secondary problems in diabetes mellitus (DM) [1, 2]. Excessive formation of early glycation products may adversely affect diabetic complications [4, 5]. Amadori-proteins are the major representative of glycation proteins’ family, most studies conducted so far have focused on the role of AGEs in diabetesrelated complications. Aminoguanidine (pimagedine, CH6N4), a prototype agent, acts by trapping or scavenging reactive carbonyl intermediates generated by the Maillard reaction, mainly hydroxyaldehydes and dicarbonyl compounds, including methylglyoxal [15, 16]. It is a highly reactive nucleophilic agent that reacts with many biological macromolecules (pyridoxal phosphate, pyruvate, glucose, malondialdehyde, and others). Levels of HbA1c and fructosamine have been estimated as markers of Amadori products
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