Cysteine Prevents the Development of Experimental Diabetes Induced by Zinc-Binding Substances
In experimental rabbits, cysteine injected intravenously in a dose of 1000 mg/kg temporarily bound zinc in β cells and prevented the formation of chelate zinc complexes in response to subsequent injection of diabetogenic zinc-binding substances that induce cell destruction. Injection of cysteine to...
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Published in | Bulletin of experimental biology and medicine Vol. 168; no. 5; pp. 621 - 626 |
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01.03.2020
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Abstract | In experimental rabbits, cysteine injected intravenously in a dose of 1000 mg/kg temporarily bound zinc in β cells and prevented the formation of chelate zinc complexes in response to subsequent injection of diabetogenic zinc-binding substances that induce cell destruction. Injection of cysteine to animals was associated with a sharply negative reaction to zinc in β cells, which attests to blockade of zinc ions. Injection of cysteine few minutes after dithizone and formation of zinc—dithizone complex was followed by displacement of dithizone from the complex and prevented the development of diabetes in most animals. The most plausible mechanism of preventive effect of cysteine is the formation of 2:1 zinc—cysteine complex in β cells with possible fixation of Zn atom between sulfur atoms from SH groups of two cysteine molecules. |
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AbstractList | In experimental rabbits, cysteine injected intravenously in a dose of 1000 mg/kg temporarily bound zinc in β cells and prevented the formation of chelate zinc complexes in response to subsequent injection of diabetogenic zinc-binding substances that induce cell destruction. Injection of cysteine to animals was associated with a sharply negative reaction to zinc in β cells, which attests to blockade of zinc ions. Injection of cysteine few minutes after dithizone and formation of zinc—dithizone complex was followed by displacement of dithizone from the complex and prevented the development of diabetes in most animals. The most plausible mechanism of preventive effect of cysteine is the formation of 2:1 zinc—cysteine complex in β cells with possible fixation of Zn atom between sulfur atoms from SH groups of two cysteine molecules. In experimental rabbits, cysteine injected intravenously in a dose of 1000 mg/kg temporarily bound zinc in [beta] cells and prevented the formation of chelate zinc complexes in response to subsequent injection of diabetogenic zinc-binding substances that induce cell destruction. Injection of cysteine to animals was associated with a sharply negative reaction to zinc in [beta] cells, which attests to blockade of zinc ions. Injection of cysteine few minutes after dithizone and formation of zinc--dithizone complex was followed by displacement of dithizone from the complex and prevented the development of diabetes in most animals. The most plausible mechanism of preventive effect of cysteine is the formation of 2:1 zinc--cysteine complex in [beta] cells with possible fixation of Zn atom between sulfur atoms from SH groups of two cysteine molecules. In experimental rabbits, cysteine injected intravenously in a dose of 1000 mg/kg temporarily bound zinc in [beta] cells and prevented the formation of chelate zinc complexes in response to subsequent injection of diabetogenic zinc-binding substances that induce cell destruction. Injection of cysteine to animals was associated with a sharply negative reaction to zinc in [beta] cells, which attests to blockade of zinc ions. Injection of cysteine few minutes after dithizone and formation of zinc--dithizone complex was followed by displacement of dithizone from the complex and prevented the development of diabetes in most animals. The most plausible mechanism of preventive effect of cysteine is the formation of 2:1 zinc--cysteine complex in [beta] cells with possible fixation of Zn atom between sulfur atoms from SH groups of two cysteine molecules. Key Words: [beta] cells; cysteine; sulfhydryl groups; diabetogenic zinc-binding substances (DZB); 8-para-toluene sulfonamide quinoline (TSQ) |
Audience | Academic |
Author | Meyramov, G. G. Meyramova, D. A. Kartbayeva, G. T. Tykezhanova, G. M. Kovalenko, O. L. Zhumagalieva, Zh. Zh Kohnert, K.-D. Starikova, A. E. Shaybek, A. Zh |
Author_xml | – sequence: 1 givenname: G. G. surname: Meyramov fullname: Meyramov, G. G. email: meyramov@mail.ru organization: Diabetologic Research Group, E. A. Buketov Karaganda State University, E. A. Buketov Karaganda State University – sequence: 2 givenname: K.-D. surname: Kohnert fullname: Kohnert, K.-D. organization: Diabetologic Research Group, E. A. Buketov Karaganda State University, Institute of Diabetes “Gerhardt Katsh” – sequence: 3 givenname: A. Zh surname: Shaybek fullname: Shaybek, A. Zh organization: Diabetologic Research Group, E. A. Buketov Karaganda State University, E. A. Buketov Karaganda State University – sequence: 4 givenname: D. A. surname: Meyramova fullname: Meyramova, D. A. organization: Diabetologic Research Group, E. A. Buketov Karaganda State University, E. A. Buketov Karaganda State University – sequence: 5 givenname: G. T. surname: Kartbayeva fullname: Kartbayeva, G. T. organization: E. A. Buketov Karaganda State University – sequence: 6 givenname: G. M. surname: Tykezhanova fullname: Tykezhanova, G. M. organization: E. A. Buketov Karaganda State University – sequence: 7 givenname: A. E. surname: Starikova fullname: Starikova, A. E. organization: E. A. Buketov Karaganda State University – sequence: 8 givenname: O. L. surname: Kovalenko fullname: Kovalenko, O. L. organization: E. A. Buketov Karaganda State University – sequence: 9 givenname: Zh. Zh surname: Zhumagalieva fullname: Zhumagalieva, Zh. Zh organization: E. A. Buketov Karaganda State University |
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Cites_doi | 10.14341/probl11516 10.1007/s12020-013-0032-x 10.1007/s10534-005-3685-y 10.3390/toxics3010020 10.14341/probl11316 10.1007/BF01003177 10.3746/pnf.2017.22.1.1 |
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Keywords | sulfhydryl groups β cells cysteine diabetogenic zinc-binding substances (DZB) 8-para-toluene sulfonamide quinoline (TSQ) |
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References | MeyramovGGMeyramovaAG8PTSQ as fluorescent reagent for revealing of Zn-ions in B-cells and as diabetogenic chelatorActa Diabetol.200340157 MeyramovaAGKohnertKDAitkulovAMAlinaARZhuzbaevaGOKystaubaevaZTAndreewaAPKovalenkoOLZhuzshasarovaAATyrzhanovaSSHigh specific fluorescent method for staining of zinc-insulin complex in pancreatic B-cellsBull. Karaganda State University.201347884 WohlrabFvon DorscheHHKrautschickISchmidtSOn the specificity of insulin staining by Victoria blue 4RHistochem. J.198517551551810.1007/BF010031771:CAS:528:DyaL28XptV0%3D RubinoFMToxicity of glutathione-binding metals: a review of targets and mechanismsToxics.201531206210.3390/toxics30100201:CAS:528:DC%2BC1cXlsFansbs%3D Meyramov GG, Meyramova AG. Prevention of diabetes induced by chelators by L-hystidine. Diabetes. 2004;52(6, Suppl. 1):583. MeyramovGGKikimbaevaAAMeyramovaAGVictoria 4R Method Staining of Insulin in B-cells of Isolated Pancreatic IsletsActa Diabetol.2003404208 MeyramovGGKikimbaevaAAMeyramovaAGFluorescent histochemical method for staining of insulin in B-cells of isolated pancreatic islets by diethylpseudoisocyanine chlorideActa Diabetol.200542166 Meyramov GG, Kohnert KD, Kikimbaeva AA, Dupont ON, Aitkulov AM, Kystaubaeva ZT, Tykezhanova GM, Turgunva LG, Laryushina EM, Abdraimova-Meyramova AG, Shaybek AS, Zhumasheva KA, Tyrshanva SS. Gluthation’ reduced form protect B-cells from destruction caused diabetogenic ligands. Diabetes. 2015;64(7, Suppl. 1):A735. Meyramova AG. Diabetogenic zinc-binding β-cytotoxic compounds. Probl. Endokrinol. 2003;49(2):8-16. Russian. DunnMFZinc-ligand interactions modulate assembly and stability of the insulin hexamer — a reviewBiometals.200518429530310.1007/s10534-005-3685-y1:CAS:528:DC%2BD2MXpvFOksbw%3D LiYVZinc and insulin in pancreatic beta-cellsEndocrine.201445217818910.1007/s12020-013-0032-x1:CAS:528:DC%2BC3sXhtlansrrJ Meyramov GG, Konert KD, Meyramova AG. Diabetogenic effect of xanthurenic acid. Probl. Endokrinol. 2001;47(1):39-44. Russian. MaretWZinc in pancreatic islet biology insulin sensitivity, and diabetesPrev. Nutr. Food.20172211810.3746/pnf.2017.22.1.11:CAS:528:DC%2BC1MXlslOhsbw%3D FM Rubino (4765_CR12) 2015; 3 GG Meyramov (4765_CR10) 2003; 40 W Maret (4765_CR5) 2017; 22 AG Meyramova (4765_CR8) 2013; 4 YV Li (4765_CR4) 2014; 45 4765_CR11 F Wohlrab (4765_CR13) 1985; 17 MF Dunn (4765_CR3) 2005; 18 4765_CR1 GG Meyramov (4765_CR6) 2005; 42 4765_CR2 4765_CR9 GG Meyramov (4765_CR7) 2003; 40 |
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Snippet | In experimental rabbits, cysteine injected intravenously in a dose of 1000 mg/kg temporarily bound zinc in β cells and prevented the formation of chelate zinc... In experimental rabbits, cysteine injected intravenously in a dose of 1000 mg/kg temporarily bound zinc in [beta] cells and prevented the formation of chelate... |
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SubjectTerms | Animals Antibiotics Beta cells Biomedical and Life Sciences Biomedicine Blood Glucose - drug effects Blood Glucose - metabolism Cell Biology Cysteine Cysteine - pharmacology Cysteine - therapeutic use Cystine Cytoprotection - drug effects Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetes Mellitus, Experimental - prevention & control Dithizone - adverse effects Dithizone - metabolism Injection Insulin-Secreting Cells - drug effects Insulin-Secreting Cells - metabolism Internal Medicine Islets of Langerhans - drug effects Islets of Langerhans - metabolism Laboratory Medicine Pathology Rabbits Sulfonamides Sulfur Thiols Zinc Zinc - metabolism |
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Title | Cysteine Prevents the Development of Experimental Diabetes Induced by Zinc-Binding Substances |
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