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Saccharomyces cerevisiae cells lacking transcription factors Skn7 or Yap1 exhibit different susceptibility to cyanidin
Anthocyanidins – the aglycone moiety of anthocyanins – are responsible for the antioxidant traits and for many of the health benefits brought by the consumption of anthocyanin-rich foods, but whether excessive anthocyanidins are deleterious to living organisms is still a matter of debate. In the pre...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7592074/ https://www.ncbi.nlm.nih.gov/pubmed/33145450 http://dx.doi.org/10.1016/j.heliyon.2020.e05352 |
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author | Ruta, Lavinia Liliana Oprea, Eliza Popa, Claudia Valentina Farcasanu, Ileana Cornelia |
author_facet | Ruta, Lavinia Liliana Oprea, Eliza Popa, Claudia Valentina Farcasanu, Ileana Cornelia |
author_sort | Ruta, Lavinia Liliana |
collection | PubMed |
description | Anthocyanidins – the aglycone moiety of anthocyanins – are responsible for the antioxidant traits and for many of the health benefits brought by the consumption of anthocyanin-rich foods, but whether excessive anthocyanidins are deleterious to living organisms is still a matter of debate. In the present study we used the model eukaryotic microorganism Saccharomyces cerevisiae to evaluate the potential toxicity of cyanidin, one of the most prevalent anthocyanidins found in berries, grapes, purple vegetables, and red wine. We found that yeast cells lacking the transcription factors responsible for regulating the response to oxidative stress – Skn7 and Yap1 – exhibited different sensitivities to cyanidin. Cells lacking the transcription factor Skn7 were sensitive to low concentrations of cyanidin, a trait that was augmented by exposure to visible light, notably blue or green light. In contrast, the growth of yeast cells devoid of Yap1 was stimulated by low concentrations, but it was impaired by high cyanidin exposure. High, but not low cyanidin was shown to induce Yap1 translocation from cytosol to nucleus, probably by generating reactive oxygen species such as H(2)O(2). Taken together, these observation suggested that Skn7 and Yap1 have complementary roles in adaptation to cyanidin stress, with Skn7 involved in adaptation to low concentrations and with Yap1 responsible for adaptation to high concentrations of cyanidin. The results imply that caution is needed when utilizing cyanidin-enriched supplements, especially when in combination with prolonged exposure to visible light. |
format | Online Article Text |
id | pubmed-7592074 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-75920742020-11-02 Saccharomyces cerevisiae cells lacking transcription factors Skn7 or Yap1 exhibit different susceptibility to cyanidin Ruta, Lavinia Liliana Oprea, Eliza Popa, Claudia Valentina Farcasanu, Ileana Cornelia Heliyon Research Article Anthocyanidins – the aglycone moiety of anthocyanins – are responsible for the antioxidant traits and for many of the health benefits brought by the consumption of anthocyanin-rich foods, but whether excessive anthocyanidins are deleterious to living organisms is still a matter of debate. In the present study we used the model eukaryotic microorganism Saccharomyces cerevisiae to evaluate the potential toxicity of cyanidin, one of the most prevalent anthocyanidins found in berries, grapes, purple vegetables, and red wine. We found that yeast cells lacking the transcription factors responsible for regulating the response to oxidative stress – Skn7 and Yap1 – exhibited different sensitivities to cyanidin. Cells lacking the transcription factor Skn7 were sensitive to low concentrations of cyanidin, a trait that was augmented by exposure to visible light, notably blue or green light. In contrast, the growth of yeast cells devoid of Yap1 was stimulated by low concentrations, but it was impaired by high cyanidin exposure. High, but not low cyanidin was shown to induce Yap1 translocation from cytosol to nucleus, probably by generating reactive oxygen species such as H(2)O(2). Taken together, these observation suggested that Skn7 and Yap1 have complementary roles in adaptation to cyanidin stress, with Skn7 involved in adaptation to low concentrations and with Yap1 responsible for adaptation to high concentrations of cyanidin. The results imply that caution is needed when utilizing cyanidin-enriched supplements, especially when in combination with prolonged exposure to visible light. Elsevier 2020-10-26 /pmc/articles/PMC7592074/ /pubmed/33145450 http://dx.doi.org/10.1016/j.heliyon.2020.e05352 Text en © 2020 The Author(s) 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 | Research Article Ruta, Lavinia Liliana Oprea, Eliza Popa, Claudia Valentina Farcasanu, Ileana Cornelia Saccharomyces cerevisiae cells lacking transcription factors Skn7 or Yap1 exhibit different susceptibility to cyanidin |
title | Saccharomyces cerevisiae cells lacking transcription factors Skn7 or Yap1 exhibit different susceptibility to cyanidin |
title_full | Saccharomyces cerevisiae cells lacking transcription factors Skn7 or Yap1 exhibit different susceptibility to cyanidin |
title_fullStr | Saccharomyces cerevisiae cells lacking transcription factors Skn7 or Yap1 exhibit different susceptibility to cyanidin |
title_full_unstemmed | Saccharomyces cerevisiae cells lacking transcription factors Skn7 or Yap1 exhibit different susceptibility to cyanidin |
title_short | Saccharomyces cerevisiae cells lacking transcription factors Skn7 or Yap1 exhibit different susceptibility to cyanidin |
title_sort | saccharomyces cerevisiae cells lacking transcription factors skn7 or yap1 exhibit different susceptibility to cyanidin |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7592074/ https://www.ncbi.nlm.nih.gov/pubmed/33145450 http://dx.doi.org/10.1016/j.heliyon.2020.e05352 |
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