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Fructose during pregnancy provokes fetal oxidative stress: The key role of the placental heme oxygenase‐1
Author(s) -
Rodrigo Silvia,
Rodríguez Lourdes,
Otero Paola,
Panadero María I.,
García Antonia,
Barbas Coral,
Roglans Núria,
Ramos Sonia,
Goya Luis,
Laguna Juan C.,
ÁlvarezMillán Juan J.,
Bocos Carlos
Publication year - 2016
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201600193
Subject(s) - oxidative stress , endocrinology , medicine , heme oxygenase , placenta , fructose , fetus , antioxidant , chemistry , heme , biology , pregnancy , biochemistry , enzyme , genetics
Scope One of the features of metabolic syndrome caused by liquid fructose intake is an impairment of redox status. We have investigated whether maternal fructose ingestion modifies the redox status in pregnant rats and their fetuses. Methods and results Fructose (10% wt/vol) in the drinking water of rats throughout gestation, leads to maternal hepatic oxidative stress. However, this change was also observed in glucose‐fed rats and, in fact, both carbohydrates produced a decrease in antioxidant enzyme activity. Surprisingly, mothers fed carbohydrates displayed low plasma lipid oxidation. In contrast, fetuses from fructose‐fed mothers showed elevated levels of plasma lipoperoxides versus fetuses from control or glucose‐fed mothers. Interestingly, a clearly augmented oxidative stress was observed in placenta of fructose‐fed mothers, accompanied by a lower expression of the transcription factor Nuclear factor‐erythroid 2‐related factor‐2 (Nrf2) and its target gene, heme oxygenase‐1 (HO‐1), a potent antioxidant molecule. Moreover, histone deacetylase 3 (HDAC3) that has been proposed to upregulate HO‐1 expression by stabilizing Nrf2, exhibited a diminished expression in placenta of fructose‐supplemented mothers. Conclusions Maternal fructose intake provoked an imbalanced redox status in placenta and a clear diminution of HO‐1 expression, which could be responsible for the augmented oxidative stress found in their fetuses.