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Vitamin C Intake Reduces the Cytotoxicity Associated with Hyperglycemia in Prediabetes and Type 2 Diabetes
Hyperglycemia leads to the formation of free radicals and advanced glycation end-products (AGEs). Antioxidants can reduce the level of protein glycation and DNA damage. In this study, we compared the levels of vitamin C intake, which is among the most abundant antioxidants obtained from diet, with t...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741954/ https://www.ncbi.nlm.nih.gov/pubmed/23984417 http://dx.doi.org/10.1155/2013/896536 |
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author | Franke, Silvia Isabel Rech Müller, Luiza Louzada Santos, Maria Carolina Fishborn, Arcênio Hermes, Liziane Molz, Patrícia Pereira, Camila Schreiner Wichmann, Francisca Maria Assmann Horta, Jorge André Maluf, Sharbel Weidner Prá, Daniel |
author_facet | Franke, Silvia Isabel Rech Müller, Luiza Louzada Santos, Maria Carolina Fishborn, Arcênio Hermes, Liziane Molz, Patrícia Pereira, Camila Schreiner Wichmann, Francisca Maria Assmann Horta, Jorge André Maluf, Sharbel Weidner Prá, Daniel |
author_sort | Franke, Silvia Isabel Rech |
collection | PubMed |
description | Hyperglycemia leads to the formation of free radicals and advanced glycation end-products (AGEs). Antioxidants can reduce the level of protein glycation and DNA damage. In this study, we compared the levels of vitamin C intake, which is among the most abundant antioxidants obtained from diet, with the levels of fasting plasma glucose (FPG), glycated hemoglobin (A1C), DNA damage, and cytotoxicity in prediabetic subjects and type 2 diabetic subjects. Our results indicated that there was no significant correlation between FPG or A1C and DNA damage parameters (micronuclei, nucleoplasmic bridges, and nuclear buds). FPG and A1C correlated with necrosis (r = 0.294; P = 0.013 and r = 0.401; P = 0.001, resp.). Vitamin C intake correlated negatively with necrosis and apoptosis (r = −0.246; P = 0.040, and r = −0.276; P = 0.021, resp.). The lack of a correlation between the FPG and A1C and DNA damage could be explained, at least in part, by the elimination of cells with DNA damage by either necrosis or apoptosis (cytotoxicity). Vitamin C appeared to improve cell survival by reducing cytotoxicity. Therefore, the present results indicate the need for clinical studies to evaluate the effect of low-dose vitamin C supplementation in type 2 diabetes. |
format | Online Article Text |
id | pubmed-3741954 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-37419542013-08-27 Vitamin C Intake Reduces the Cytotoxicity Associated with Hyperglycemia in Prediabetes and Type 2 Diabetes Franke, Silvia Isabel Rech Müller, Luiza Louzada Santos, Maria Carolina Fishborn, Arcênio Hermes, Liziane Molz, Patrícia Pereira, Camila Schreiner Wichmann, Francisca Maria Assmann Horta, Jorge André Maluf, Sharbel Weidner Prá, Daniel Biomed Res Int Research Article Hyperglycemia leads to the formation of free radicals and advanced glycation end-products (AGEs). Antioxidants can reduce the level of protein glycation and DNA damage. In this study, we compared the levels of vitamin C intake, which is among the most abundant antioxidants obtained from diet, with the levels of fasting plasma glucose (FPG), glycated hemoglobin (A1C), DNA damage, and cytotoxicity in prediabetic subjects and type 2 diabetic subjects. Our results indicated that there was no significant correlation between FPG or A1C and DNA damage parameters (micronuclei, nucleoplasmic bridges, and nuclear buds). FPG and A1C correlated with necrosis (r = 0.294; P = 0.013 and r = 0.401; P = 0.001, resp.). Vitamin C intake correlated negatively with necrosis and apoptosis (r = −0.246; P = 0.040, and r = −0.276; P = 0.021, resp.). The lack of a correlation between the FPG and A1C and DNA damage could be explained, at least in part, by the elimination of cells with DNA damage by either necrosis or apoptosis (cytotoxicity). Vitamin C appeared to improve cell survival by reducing cytotoxicity. Therefore, the present results indicate the need for clinical studies to evaluate the effect of low-dose vitamin C supplementation in type 2 diabetes. Hindawi Publishing Corporation 2013 2013-07-25 /pmc/articles/PMC3741954/ /pubmed/23984417 http://dx.doi.org/10.1155/2013/896536 Text en Copyright © 2013 Silvia Isabel Rech Franke et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Franke, Silvia Isabel Rech Müller, Luiza Louzada Santos, Maria Carolina Fishborn, Arcênio Hermes, Liziane Molz, Patrícia Pereira, Camila Schreiner Wichmann, Francisca Maria Assmann Horta, Jorge André Maluf, Sharbel Weidner Prá, Daniel Vitamin C Intake Reduces the Cytotoxicity Associated with Hyperglycemia in Prediabetes and Type 2 Diabetes |
title | Vitamin C Intake Reduces the Cytotoxicity Associated with Hyperglycemia in Prediabetes and Type 2 Diabetes |
title_full | Vitamin C Intake Reduces the Cytotoxicity Associated with Hyperglycemia in Prediabetes and Type 2 Diabetes |
title_fullStr | Vitamin C Intake Reduces the Cytotoxicity Associated with Hyperglycemia in Prediabetes and Type 2 Diabetes |
title_full_unstemmed | Vitamin C Intake Reduces the Cytotoxicity Associated with Hyperglycemia in Prediabetes and Type 2 Diabetes |
title_short | Vitamin C Intake Reduces the Cytotoxicity Associated with Hyperglycemia in Prediabetes and Type 2 Diabetes |
title_sort | vitamin c intake reduces the cytotoxicity associated with hyperglycemia in prediabetes and type 2 diabetes |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741954/ https://www.ncbi.nlm.nih.gov/pubmed/23984417 http://dx.doi.org/10.1155/2013/896536 |
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