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Research ArticleOpen Access

Prevention Destruction of Pancreatic B-Cells Caused “by Diabetogenic Zinc-binding chemicals by Amino acids Contains of SH-Radical in Structure of Molecule

Volume 9 - Issue 3

Meyramov GG*, Shaybek AS and Dupont ON

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    • Diabetes Research Group, Karaganda State Medical University, Russia

    *Corresponding author: Gabit G Meyramov, Diabetes Research Group, Karaganda State Medical University Karaganda, Kazakhstan, Russia

Received: September 10, 2018;   Published: October 01, 2018

DOI: 10.26717/BJSTR.2018.09.001811

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Authors investigated toxic properties of diabetogenic derivatives of 8-hydroxyquinoline (8-OX) and of Diphenyl thiocarbazone (DZ) on the insulin producing cells of the pancreas and the protective effect of Glutathione on its toxic action. The mechanism of action of derivatives of 8-OX determined by the ability to form into cells containing zinc-ions a chelate salts with them 1:1 by sulfur and nitrogen atoms at positions 8 and 1 and through the oxygen atoms in positions 8 and 2. Diphenyl thiocarbazone formed chelates salts with zinc as 2:1, where in zinc coupled to the two atoms via Dithizone sulfur and nitrogen atoms. It is shown that the preventing effect has GRF, containing in structure of SH-radical unlike GOF, not containing it. It is found that administration of CRF to animals 1000mg/kg comp- letely protect B-cells of destruction determined by blocking of zinc by CRF. Results showed that this effect determined by blocking of zinc in B-cells by GRF. Authors suggest that atom of Zinc is fixed between atom of sulfur of the SH-radical and of atom of oxygen or nitrogen as after injections of 8-OX or DZ islet zinc binding too through atom of sulfur and oxygen.

Keywords: B-cells; Reduced form of Glutathione; Insulin; Zinc; Experimental Diabetes

Abbreviations: Zn: Zinc; DZ: Diphenylthiocarbazone (Dithizon); 8PTSQ: 8 para(toluenesulphonylmino)quinolin; GRF: Reduced form of Glutathione; GOF: Oxidized form of Glutathione

Abstract | Introduction | Methods | Results| Discussion| Conclusion| References|