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A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes

Dimethyl sulfoxide (DMSO) is an effective solvent and cytoprotectant agent that can induce diverse actions in experimental settings, ranging from metabolic stress to cytotoxic effects depending on the concentration used. Therefore, for the quality of experiments and reproducibility of results it is...

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Autores principales: Dludla, Phiwayinkosi V., Jack, Babalwa, Viraragavan, Amsha, Pheiffer, Carmen, Johnson, Rabia, Louw, Johan, Muller, Christo J.F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197677/
https://www.ncbi.nlm.nih.gov/pubmed/30364542
http://dx.doi.org/10.1016/j.toxrep.2018.10.002
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author Dludla, Phiwayinkosi V.
Jack, Babalwa
Viraragavan, Amsha
Pheiffer, Carmen
Johnson, Rabia
Louw, Johan
Muller, Christo J.F.
author_facet Dludla, Phiwayinkosi V.
Jack, Babalwa
Viraragavan, Amsha
Pheiffer, Carmen
Johnson, Rabia
Louw, Johan
Muller, Christo J.F.
author_sort Dludla, Phiwayinkosi V.
collection PubMed
description Dimethyl sulfoxide (DMSO) is an effective solvent and cytoprotectant agent that can induce diverse actions in experimental settings, ranging from metabolic stress to cytotoxic effects depending on the concentration used. Therefore, for the quality of experiments and reproducibility of results it is essential to establish a precise and non-toxic dose of DMSO within a specific cell system. 3T3-L1 adipocytes, represent a well-established in vitro cell model used to assess the anti-obesity potential of extracts and compounds. Although DMSO is commonly used as a solvent for these experiments, there is limited data available on the compounding effects of using DMSO. The purpose of this study was to assess a concentration-dependent effect of DMSO on lipid content, cell viability and oxidative damage in 3T3-L1 adipocytes. Results showed that DMSO at doses ≥ 0.1% increased mitochondrial membrane potential as measured by JC-1 fluorescent staining, while doses ≥ 10% reduced the lipid content in matured adipocytes. Consistently, higher doses significantly reduced cell viability, elevated reactive oxygen species levels, depleted intracellular glutathione levels, and accelerated apoptosis and cell necrosis. An interesting finding was that a DMSO dose of 0.01% improved glutathione content of 3T3-L1 adipocytes and had minimal effects on cell viability, apoptosis or and necrosis, supporting its antioxidant effect. Therefore, this study provides compelling evidence that precaution should be taken when assessing compounds dissolved in DMSO, particularly doses ≥1% that were shown to induce oxidative stress in 3T3-L1 adipocytes.
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spelling pubmed-61976772018-10-24 A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes Dludla, Phiwayinkosi V. Jack, Babalwa Viraragavan, Amsha Pheiffer, Carmen Johnson, Rabia Louw, Johan Muller, Christo J.F. Toxicol Rep Article Dimethyl sulfoxide (DMSO) is an effective solvent and cytoprotectant agent that can induce diverse actions in experimental settings, ranging from metabolic stress to cytotoxic effects depending on the concentration used. Therefore, for the quality of experiments and reproducibility of results it is essential to establish a precise and non-toxic dose of DMSO within a specific cell system. 3T3-L1 adipocytes, represent a well-established in vitro cell model used to assess the anti-obesity potential of extracts and compounds. Although DMSO is commonly used as a solvent for these experiments, there is limited data available on the compounding effects of using DMSO. The purpose of this study was to assess a concentration-dependent effect of DMSO on lipid content, cell viability and oxidative damage in 3T3-L1 adipocytes. Results showed that DMSO at doses ≥ 0.1% increased mitochondrial membrane potential as measured by JC-1 fluorescent staining, while doses ≥ 10% reduced the lipid content in matured adipocytes. Consistently, higher doses significantly reduced cell viability, elevated reactive oxygen species levels, depleted intracellular glutathione levels, and accelerated apoptosis and cell necrosis. An interesting finding was that a DMSO dose of 0.01% improved glutathione content of 3T3-L1 adipocytes and had minimal effects on cell viability, apoptosis or and necrosis, supporting its antioxidant effect. Therefore, this study provides compelling evidence that precaution should be taken when assessing compounds dissolved in DMSO, particularly doses ≥1% that were shown to induce oxidative stress in 3T3-L1 adipocytes. Elsevier 2018-10-04 /pmc/articles/PMC6197677/ /pubmed/30364542 http://dx.doi.org/10.1016/j.toxrep.2018.10.002 Text en © 2018 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Dludla, Phiwayinkosi V.
Jack, Babalwa
Viraragavan, Amsha
Pheiffer, Carmen
Johnson, Rabia
Louw, Johan
Muller, Christo J.F.
A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes
title A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes
title_full A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes
title_fullStr A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes
title_full_unstemmed A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes
title_short A dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3T3-L1 adipocytes
title_sort dose-dependent effect of dimethyl sulfoxide on lipid content, cell viability and oxidative stress in 3t3-l1 adipocytes
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197677/
https://www.ncbi.nlm.nih.gov/pubmed/30364542
http://dx.doi.org/10.1016/j.toxrep.2018.10.002
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