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Therapeutic concentration of morphine reduces oxidative stress in glioma cell line

Morphine is a potent analgesic opioid used extensively for pain treatment. During the last decade, global consumption grew more than 4-fold. However, molecular mechanisms elicited by morphine are not totally understood. Thus, a growing literature indicates that there are additional actions to the an...

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Autores principales: Almeida, M.B., Costa-Malaquias, A., Nascimento, J.L.M., Oliveira, K.R., Herculano, A.M., Crespo-López, M.E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Associação Brasileira de Divulgação Científica 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4075308/
https://www.ncbi.nlm.nih.gov/pubmed/24728211
http://dx.doi.org/10.1590/1414-431X20143697
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author Almeida, M.B.
Costa-Malaquias, A.
Nascimento, J.L.M.
Oliveira, K.R.
Herculano, A.M.
Crespo-López, M.E.
author_facet Almeida, M.B.
Costa-Malaquias, A.
Nascimento, J.L.M.
Oliveira, K.R.
Herculano, A.M.
Crespo-López, M.E.
author_sort Almeida, M.B.
collection PubMed
description Morphine is a potent analgesic opioid used extensively for pain treatment. During the last decade, global consumption grew more than 4-fold. However, molecular mechanisms elicited by morphine are not totally understood. Thus, a growing literature indicates that there are additional actions to the analgesic effect. Previous studies about morphine and oxidative stress are controversial and used concentrations outside the range of clinical practice. Therefore, in this study, we hypothesized that a therapeutic concentration of morphine (1 μM) would show a protective effect in a traditional model of oxidative stress. We exposed the C6 glioma cell line to hydrogen peroxide (H(2)O(2)) and/or morphine for 24 h and evaluated cell viability, lipid peroxidation, and levels of sulfhydryl groups (an indicator of the redox state of the cell). Morphine did not prevent the decrease in cell viability provoked by H(2)O(2) but partially prevented lipid peroxidation caused by 0.0025% H(2)O(2) (a concentration allowing more than 90% cell viability). Interestingly, this opioid did not alter the increased levels of sulfhydryl groups produced by exposure to 0.0025% H(2)O(2), opening the possibility that alternative molecular mechanisms (a direct scavenging activity or the inhibition of NAPDH oxidase) may explain the protective effect registered in the lipid peroxidation assay. Our results demonstrate, for the first time, that morphine in usual analgesic doses may contribute to minimizing oxidative stress in cells of glial origin. This study supports the importance of employing concentrations similar to those used in clinical practice for a better approximation between experimental models and the clinical setting.
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spelling pubmed-40753082014-07-09 Therapeutic concentration of morphine reduces oxidative stress in glioma cell line Almeida, M.B. Costa-Malaquias, A. Nascimento, J.L.M. Oliveira, K.R. Herculano, A.M. Crespo-López, M.E. Braz J Med Biol Res Biomedical Sciences Morphine is a potent analgesic opioid used extensively for pain treatment. During the last decade, global consumption grew more than 4-fold. However, molecular mechanisms elicited by morphine are not totally understood. Thus, a growing literature indicates that there are additional actions to the analgesic effect. Previous studies about morphine and oxidative stress are controversial and used concentrations outside the range of clinical practice. Therefore, in this study, we hypothesized that a therapeutic concentration of morphine (1 μM) would show a protective effect in a traditional model of oxidative stress. We exposed the C6 glioma cell line to hydrogen peroxide (H(2)O(2)) and/or morphine for 24 h and evaluated cell viability, lipid peroxidation, and levels of sulfhydryl groups (an indicator of the redox state of the cell). Morphine did not prevent the decrease in cell viability provoked by H(2)O(2) but partially prevented lipid peroxidation caused by 0.0025% H(2)O(2) (a concentration allowing more than 90% cell viability). Interestingly, this opioid did not alter the increased levels of sulfhydryl groups produced by exposure to 0.0025% H(2)O(2), opening the possibility that alternative molecular mechanisms (a direct scavenging activity or the inhibition of NAPDH oxidase) may explain the protective effect registered in the lipid peroxidation assay. Our results demonstrate, for the first time, that morphine in usual analgesic doses may contribute to minimizing oxidative stress in cells of glial origin. This study supports the importance of employing concentrations similar to those used in clinical practice for a better approximation between experimental models and the clinical setting. Associação Brasileira de Divulgação Científica 2014-04-11 /pmc/articles/PMC4075308/ /pubmed/24728211 http://dx.doi.org/10.1590/1414-431X20143697 Text en http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Biomedical Sciences
Almeida, M.B.
Costa-Malaquias, A.
Nascimento, J.L.M.
Oliveira, K.R.
Herculano, A.M.
Crespo-López, M.E.
Therapeutic concentration of morphine reduces oxidative stress in glioma cell line
title Therapeutic concentration of morphine reduces oxidative stress in glioma cell line
title_full Therapeutic concentration of morphine reduces oxidative stress in glioma cell line
title_fullStr Therapeutic concentration of morphine reduces oxidative stress in glioma cell line
title_full_unstemmed Therapeutic concentration of morphine reduces oxidative stress in glioma cell line
title_short Therapeutic concentration of morphine reduces oxidative stress in glioma cell line
title_sort therapeutic concentration of morphine reduces oxidative stress in glioma cell line
topic Biomedical Sciences
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4075308/
https://www.ncbi.nlm.nih.gov/pubmed/24728211
http://dx.doi.org/10.1590/1414-431X20143697
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