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Effect of poly(amido)amine (PAMAM) G4 dendrimer on heart and liver mitochondria in an animal model of diabetes

Authors

  • Magdalena Labieniec,

    Corresponding author
    1. Department of General Biophysics, University of Lodz, 12/16 Banacha Street, 90-237 Lodz, Poland
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  • Olga Ulicna,

    1. Pharmacobiochemical Laboratory, 3rd Department of Internal Medicine, Faculty of Medicine, Comenius University, 7 Hlboka Street, 811 05 Bratislava, Slovakia
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  • Olga Vancova,

    1. Pharmacobiochemical Laboratory, 3rd Department of Internal Medicine, Faculty of Medicine, Comenius University, 7 Hlboka Street, 811 05 Bratislava, Slovakia
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  • Jarmila Kucharska,

    1. Pharmacobiochemical Laboratory, 3rd Department of Internal Medicine, Faculty of Medicine, Comenius University, 7 Hlboka Street, 811 05 Bratislava, Slovakia
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  • Teresa Gabryelak,

    1. Department of General Biophysics, University of Lodz, 12/16 Banacha Street, 90-237 Lodz, Poland
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  • Cezary Watala

    1. Department of Haemostasis and Haemostatic Disorders, Medical University of Lodz, University Clinical Hospital No 2, 113 Zeromski Street, 90-549 Lodz, Poland
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email magdalab@biol.uni.lodz.pl

Abstract

Diabetes-induced injury related to hyperglycaemia is associated with impaired function of mitochondria. Regardless of their cytotoxicity, PAMAM [poly(amido)amine] G4 dendrimers lower plasma glucose and suppress long-term markers of diabetic hyperglycaemia in experimental diabetes. In the present study, we aimed at verifying whether such modulatory effects of PAMAM G4 (0.5 μmol/kg of body weight daily for 60 days) may contribute to improved respiration in heart and liver mitochondria from streptozotocin-diabetic rats. PAMAM G4 alleviated long-term markers of hyperglycaemia and reduced blood and tissue lipophilic antioxidants in diabetic animals, but did not restore mitochondrial function. In hearts, but not livers, dendrimers further reduced respiratory function and oxidative phosphorylation. Thus ameliorating effects of PAMAM G4 on glycation and glycoxidation in experimental diabetes are not sufficient to restore the impaired mitochondrial function in diabetes.

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