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Biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain
Aspartame, an artificial sweetener, is very widely used in many foods and beverages. But there are controversies about its metabolite which is marked for its toxicity. Hence it is believed to be unsafe for human use. Previous studies have reported on methanol exposure with involvements of free radic...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4085354/ https://www.ncbi.nlm.nih.gov/pubmed/25009784 http://dx.doi.org/10.1016/j.redox.2014.04.011 |
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author | Ashok, Iyaswamy Sheeladevi, Rathinasamy |
author_facet | Ashok, Iyaswamy Sheeladevi, Rathinasamy |
author_sort | Ashok, Iyaswamy |
collection | PubMed |
description | Aspartame, an artificial sweetener, is very widely used in many foods and beverages. But there are controversies about its metabolite which is marked for its toxicity. Hence it is believed to be unsafe for human use. Previous studies have reported on methanol exposure with involvements of free radicals on excitotoxicity of neuronal apoptosis. Hence, this present study is proposed to investigate whether or not chronic aspartame (FDA approved Daily Acceptable Intake (ADI),40 mg/kg bwt) administration could release methanol, and whether or not it can induce changes in brain oxidative stress status and gene and protein expression of anti-apoptotic Bcl-2 and pro-apoptotic Bax and caspase-3 in the rat brain region. To mimic the human methanol metabolism, Methotrexate (MTX)-treated Wistar strain male albino rats were used and after the oral administration of aspartame, the effects were studied along with controls and MTX-treated controls. Aspartame exposure resulted with a significant increase in the enzymatic activity in protein carbonyl, lipid peroxidation levels, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase and catalase activity in (aspartame MTX)-treated animals and with a significant decrease in reduced glutathione, glutathione reductase and protein thiol, pointing out the generation of free radicals. The gene and protein expression of pro apoptotic marker Bax showed a marked increase whereas the anti-apoptotic marker Bcl-2 decreased markedly indicating the aspartame is harmful at cellular level. It is clear that long term aspartame exposure could alter the brain antioxidant status, and can induce apoptotic changes in brain. |
format | Online Article Text |
id | pubmed-4085354 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-40853542014-07-09 Biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain Ashok, Iyaswamy Sheeladevi, Rathinasamy Redox Biol Research Paper Aspartame, an artificial sweetener, is very widely used in many foods and beverages. But there are controversies about its metabolite which is marked for its toxicity. Hence it is believed to be unsafe for human use. Previous studies have reported on methanol exposure with involvements of free radicals on excitotoxicity of neuronal apoptosis. Hence, this present study is proposed to investigate whether or not chronic aspartame (FDA approved Daily Acceptable Intake (ADI),40 mg/kg bwt) administration could release methanol, and whether or not it can induce changes in brain oxidative stress status and gene and protein expression of anti-apoptotic Bcl-2 and pro-apoptotic Bax and caspase-3 in the rat brain region. To mimic the human methanol metabolism, Methotrexate (MTX)-treated Wistar strain male albino rats were used and after the oral administration of aspartame, the effects were studied along with controls and MTX-treated controls. Aspartame exposure resulted with a significant increase in the enzymatic activity in protein carbonyl, lipid peroxidation levels, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase and catalase activity in (aspartame MTX)-treated animals and with a significant decrease in reduced glutathione, glutathione reductase and protein thiol, pointing out the generation of free radicals. The gene and protein expression of pro apoptotic marker Bax showed a marked increase whereas the anti-apoptotic marker Bcl-2 decreased markedly indicating the aspartame is harmful at cellular level. It is clear that long term aspartame exposure could alter the brain antioxidant status, and can induce apoptotic changes in brain. Elsevier 2014-04-29 /pmc/articles/PMC4085354/ /pubmed/25009784 http://dx.doi.org/10.1016/j.redox.2014.04.011 Text en © 2014 The Authors http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/). |
spellingShingle | Research Paper Ashok, Iyaswamy Sheeladevi, Rathinasamy Biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain |
title | Biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain |
title_full | Biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain |
title_fullStr | Biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain |
title_full_unstemmed | Biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain |
title_short | Biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain |
title_sort | biochemical responses and mitochondrial mediated activation of apoptosis on long-term effect of aspartame in rat brain |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4085354/ https://www.ncbi.nlm.nih.gov/pubmed/25009784 http://dx.doi.org/10.1016/j.redox.2014.04.011 |
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