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Protection of Renal Tubular Cells by Antioxidants: Current Knowledge and New Trends

Acute renal damage mainly develops following toxic or ischemic insults and is defined as acute. These damages have largely been attributed to oxidative stress. Recently much attention has been directed toward decreased renal tubular cell regeneration during tubular cell injury. Antioxidants have rec...

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Autores principales: Baradaran, Azar, Nasri, Hamid, Rafieian-Kopaei, Mahmoud
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Royan Institute 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297497/
https://www.ncbi.nlm.nih.gov/pubmed/25685748
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author Baradaran, Azar
Nasri, Hamid
Rafieian-Kopaei, Mahmoud
author_facet Baradaran, Azar
Nasri, Hamid
Rafieian-Kopaei, Mahmoud
author_sort Baradaran, Azar
collection PubMed
description Acute renal damage mainly develops following toxic or ischemic insults and is defined as acute. These damages have largely been attributed to oxidative stress. Recently much attention has been directed toward decreased renal tubular cell regeneration during tubular cell injury. Antioxidants have recently been the focus of researchers and scientists for prevention and treatment of various oxidative stress-related conditions, including renal toxicities. Although free radicals are known to contribute in kidney injury and abundant researches, particularly laboratory trials, have shown the beneficial effects of antioxidants against these complications, long term clinical trials do not uniformly confirm this matter, especially for single antioxidant consumption such as vitamin C. The aim of this paper is to discuss the possible explanation of this matter.
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spelling pubmed-42974972015-02-13 Protection of Renal Tubular Cells by Antioxidants: Current Knowledge and New Trends Baradaran, Azar Nasri, Hamid Rafieian-Kopaei, Mahmoud Cell J Letter to The Editor Acute renal damage mainly develops following toxic or ischemic insults and is defined as acute. These damages have largely been attributed to oxidative stress. Recently much attention has been directed toward decreased renal tubular cell regeneration during tubular cell injury. Antioxidants have recently been the focus of researchers and scientists for prevention and treatment of various oxidative stress-related conditions, including renal toxicities. Although free radicals are known to contribute in kidney injury and abundant researches, particularly laboratory trials, have shown the beneficial effects of antioxidants against these complications, long term clinical trials do not uniformly confirm this matter, especially for single antioxidant consumption such as vitamin C. The aim of this paper is to discuss the possible explanation of this matter. Royan Institute 2015 2015-01-13 /pmc/articles/PMC4297497/ /pubmed/25685748 Text en Any use, distribution, reproduction or abstract of this publication in any medium, with the exception of commercial purposes, is permitted provided the original work is properly cited http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Letter to The Editor
Baradaran, Azar
Nasri, Hamid
Rafieian-Kopaei, Mahmoud
Protection of Renal Tubular Cells by Antioxidants: Current Knowledge and New Trends
title Protection of Renal Tubular Cells by Antioxidants: Current Knowledge and New Trends
title_full Protection of Renal Tubular Cells by Antioxidants: Current Knowledge and New Trends
title_fullStr Protection of Renal Tubular Cells by Antioxidants: Current Knowledge and New Trends
title_full_unstemmed Protection of Renal Tubular Cells by Antioxidants: Current Knowledge and New Trends
title_short Protection of Renal Tubular Cells by Antioxidants: Current Knowledge and New Trends
title_sort protection of renal tubular cells by antioxidants: current knowledge and new trends
topic Letter to The Editor
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297497/
https://www.ncbi.nlm.nih.gov/pubmed/25685748
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