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Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains

Antioxidant defences are comparatively low during foetal development making the brain particularly susceptible to oxidative stress during antioxidant deficiencies. The brain is one of the organs containing the highest concentration of vitamin C (VitC) and VitC deficiency during foetal development ma...

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Autores principales: Paidi, Maya D., Schjoldager, Janne G., Lykkesfeldt, Jens, Tveden-Nyborg, Pernille
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3926113/
https://www.ncbi.nlm.nih.gov/pubmed/24563854
http://dx.doi.org/10.1016/j.redox.2014.01.009
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author Paidi, Maya D.
Schjoldager, Janne G.
Lykkesfeldt, Jens
Tveden-Nyborg, Pernille
author_facet Paidi, Maya D.
Schjoldager, Janne G.
Lykkesfeldt, Jens
Tveden-Nyborg, Pernille
author_sort Paidi, Maya D.
collection PubMed
description Antioxidant defences are comparatively low during foetal development making the brain particularly susceptible to oxidative stress during antioxidant deficiencies. The brain is one of the organs containing the highest concentration of vitamin C (VitC) and VitC deficiency during foetal development may place the brain at risk of redox status imbalance. In the present study, we investigated the developmental pattern and effect of VitC deficiency on antioxidants, vitamin E and superoxide dismutase (SOD), assessed oxidative damage by measuring malondialdehyde (MDA), hydroxynonenal (HNE) and nitrotyrosine (NT) and analysed gene and protein expression of apoptosis marker caspase-3 in the guinea pig foetal brain at two gestational (GD) time points, GD 45/pre-term and GD 56/near term following either a VitC sufficient (CTRL) or deficient (DEF) maternal dietary regime. We show that except for SOD, antioxidants and oxidative damage markers are differentially expressed between the two GDs, with high VitC (p<0.0001), NT modified proteins (p<0.0001) and active caspase-3 levels (p<0.05) at pre-term and high vitamin E levels (p<0.0001), HNE (p<0.0001) and MDA (p<0.0001) at near term. VitC deficiency significantly increased SOD activity (p<0.0001) compared to CTRLs at both GDs indicating a compensatory response, however, low levels of VitC significantly elevated MDA levels (p<0.05) in DEF at near term. Our results show a differential regulation of the investigated markers during late gestation and suggest that immature brains are susceptible to oxidative stress due to prenatal vitC deficiency in spite of an induction of protective adaptation mechanisms.
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spelling pubmed-39261132014-02-21 Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains Paidi, Maya D. Schjoldager, Janne G. Lykkesfeldt, Jens Tveden-Nyborg, Pernille Redox Biol Research Papers Antioxidant defences are comparatively low during foetal development making the brain particularly susceptible to oxidative stress during antioxidant deficiencies. The brain is one of the organs containing the highest concentration of vitamin C (VitC) and VitC deficiency during foetal development may place the brain at risk of redox status imbalance. In the present study, we investigated the developmental pattern and effect of VitC deficiency on antioxidants, vitamin E and superoxide dismutase (SOD), assessed oxidative damage by measuring malondialdehyde (MDA), hydroxynonenal (HNE) and nitrotyrosine (NT) and analysed gene and protein expression of apoptosis marker caspase-3 in the guinea pig foetal brain at two gestational (GD) time points, GD 45/pre-term and GD 56/near term following either a VitC sufficient (CTRL) or deficient (DEF) maternal dietary regime. We show that except for SOD, antioxidants and oxidative damage markers are differentially expressed between the two GDs, with high VitC (p<0.0001), NT modified proteins (p<0.0001) and active caspase-3 levels (p<0.05) at pre-term and high vitamin E levels (p<0.0001), HNE (p<0.0001) and MDA (p<0.0001) at near term. VitC deficiency significantly increased SOD activity (p<0.0001) compared to CTRLs at both GDs indicating a compensatory response, however, low levels of VitC significantly elevated MDA levels (p<0.05) in DEF at near term. Our results show a differential regulation of the investigated markers during late gestation and suggest that immature brains are susceptible to oxidative stress due to prenatal vitC deficiency in spite of an induction of protective adaptation mechanisms. Elsevier 2014-01-20 /pmc/articles/PMC3926113/ /pubmed/24563854 http://dx.doi.org/10.1016/j.redox.2014.01.009 Text en © 2014 The Authors https://creativecommons.org/licenses/by-nc-nd/3.0/This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License (https://creativecommons.org/licenses/by-nc-nd/3.0/) .
spellingShingle Research Papers
Paidi, Maya D.
Schjoldager, Janne G.
Lykkesfeldt, Jens
Tveden-Nyborg, Pernille
Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains
title Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains
title_full Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains
title_fullStr Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains
title_full_unstemmed Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains
title_short Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains
title_sort prenatal vitamin c deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains
topic Research Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3926113/
https://www.ncbi.nlm.nih.gov/pubmed/24563854
http://dx.doi.org/10.1016/j.redox.2014.01.009
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