ArticlePloS one2022
Attenuation of hyperglycemia and amadori products by aminoguanidine in alloxan-diabetic rabbits occurs via enhancement in antioxidant defenses and control of stress.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- The Effect of Aminoguanidine on Fibrinogen Gene Expression and Oxidative Stress Biomarkers in the Liver Tissue of a Streptozotocin-Induced Diabetic Rat ModelTurkish journal of pharmaceutical sciences · 2026Article
- Aminoguanidine attenuates arsenic-induced hepatic oxidative stress: Dose-dependent effects in a mouse model.Toxicology reports · 2025Article
- Effects ofPharmaceuticals (Basel, Switzerland) · 2025Article
- Elevated Oxidative Stress in Patients with Coexisting Multiple Sclerosis and Migraine: A Cross-Sectional Study.Antioxidants (Basel, Switzerland) · 2025Article
- Mitigating diabetes associated with reactive oxygen species (ROS) and protein aggregation through pharmacological interventions.RSC advances · 2024Review
- The Role of Oxidative Stress-Mediated Inflammation in the Development of T2DM-Induced Diabetic Nephropathy: Possible Preventive Action of Tannins and Other Oligomeric Polyphenols.Molecules (Basel, Switzerland) · 2022Review
- The Role of Oxidative Stress in Atopic Dermatitis and Chronic Urticaria.Antioxidants (Basel, Switzerland) · 2022Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
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.
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