Resveratrol prevents ammonia toxicity in astroglial cells.
Ammonia is implicated as a neurotoxin in brain metabolic disorders associated with hyperammonemia. Acute ammonia toxicity can be mediated by an excitotoxic mechanism, oxidative stress and nitric oxide (NO) production. Astrocytes interact with neurons, providing metabolic support and protecting again...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2012-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3528750?pdf=render |
| _version_ | 1811310394859323392 |
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| author | Larissa Daniele Bobermin André Quincozes-Santos Maria Cristina Guerra Marina Concli Leite Diogo Onofre Souza Carlos-Alberto Gonçalves Carmem Gottfried |
| author_facet | Larissa Daniele Bobermin André Quincozes-Santos Maria Cristina Guerra Marina Concli Leite Diogo Onofre Souza Carlos-Alberto Gonçalves Carmem Gottfried |
| author_sort | Larissa Daniele Bobermin |
| collection | DOAJ |
| description | Ammonia is implicated as a neurotoxin in brain metabolic disorders associated with hyperammonemia. Acute ammonia toxicity can be mediated by an excitotoxic mechanism, oxidative stress and nitric oxide (NO) production. Astrocytes interact with neurons, providing metabolic support and protecting against oxidative stress and excitotoxicity. Astrocytes also convert excess ammonia and glutamate into glutamine via glutamine synthetase (GS). Resveratrol, a polyphenol found in grapes and red wines, exhibits antioxidant and anti-inflammatory properties and modulates glial functions, such as glutamate metabolism. We investigated the effect of resveratrol on the production of reactive oxygen species (ROS), GS activity, S100B secretion, TNF-α, IL-1β and IL-6 levels in astroglial cells exposed to ammonia. Ammonia induced oxidative stress, decreased GS activity and increased cytokines release, probably by a mechanism dependent on protein kinase A (PKA) and extracellular signal-regulated kinase (ERK) pathways. Resveratrol prevented ammonia toxicity by modulating oxidative stress, glial and inflammatory responses. The ERK and nuclear factor-κB (NF-κB) are involved in the protective effect of resveratrol on cytokines proinflammatory release. In contrast, other antioxidants (e.g., ascorbic acid and trolox) were not effective against hyperammonemia. Thus, resveratrol could be used to protect against ammonia-induced neurotoxicity. |
| first_indexed | 2024-04-13T09:58:09Z |
| format | Article |
| id | doaj.art-0aed4e5bc8b442099703dcd1981c7503 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-13T09:58:09Z |
| publishDate | 2012-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-0aed4e5bc8b442099703dcd1981c75032022-12-22T02:51:18ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-01712e5216410.1371/journal.pone.0052164Resveratrol prevents ammonia toxicity in astroglial cells.Larissa Daniele BoberminAndré Quincozes-SantosMaria Cristina GuerraMarina Concli LeiteDiogo Onofre SouzaCarlos-Alberto GonçalvesCarmem GottfriedAmmonia is implicated as a neurotoxin in brain metabolic disorders associated with hyperammonemia. Acute ammonia toxicity can be mediated by an excitotoxic mechanism, oxidative stress and nitric oxide (NO) production. Astrocytes interact with neurons, providing metabolic support and protecting against oxidative stress and excitotoxicity. Astrocytes also convert excess ammonia and glutamate into glutamine via glutamine synthetase (GS). Resveratrol, a polyphenol found in grapes and red wines, exhibits antioxidant and anti-inflammatory properties and modulates glial functions, such as glutamate metabolism. We investigated the effect of resveratrol on the production of reactive oxygen species (ROS), GS activity, S100B secretion, TNF-α, IL-1β and IL-6 levels in astroglial cells exposed to ammonia. Ammonia induced oxidative stress, decreased GS activity and increased cytokines release, probably by a mechanism dependent on protein kinase A (PKA) and extracellular signal-regulated kinase (ERK) pathways. Resveratrol prevented ammonia toxicity by modulating oxidative stress, glial and inflammatory responses. The ERK and nuclear factor-κB (NF-κB) are involved in the protective effect of resveratrol on cytokines proinflammatory release. In contrast, other antioxidants (e.g., ascorbic acid and trolox) were not effective against hyperammonemia. Thus, resveratrol could be used to protect against ammonia-induced neurotoxicity.http://europepmc.org/articles/PMC3528750?pdf=render |
| spellingShingle | Larissa Daniele Bobermin André Quincozes-Santos Maria Cristina Guerra Marina Concli Leite Diogo Onofre Souza Carlos-Alberto Gonçalves Carmem Gottfried Resveratrol prevents ammonia toxicity in astroglial cells. PLoS ONE |
| title | Resveratrol prevents ammonia toxicity in astroglial cells. |
| title_full | Resveratrol prevents ammonia toxicity in astroglial cells. |
| title_fullStr | Resveratrol prevents ammonia toxicity in astroglial cells. |
| title_full_unstemmed | Resveratrol prevents ammonia toxicity in astroglial cells. |
| title_short | Resveratrol prevents ammonia toxicity in astroglial cells. |
| title_sort | resveratrol prevents ammonia toxicity in astroglial cells |
| url | http://europepmc.org/articles/PMC3528750?pdf=render |
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