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Pediatr Res. 2013 May;73(5):578-84. doi: 10.1038/pr.2013.22. Epub 2013 Feb 5.

Insufficient ascorbic acid intake during gestation induces abnormal cardiac dilation in fetal and neonatal SMP30/GNL knockout mice.

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Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.



Despite the acknowledged importance of ascorbic acid (AA) in maintaining pregnancy and normal fetal development, its precise actions remain obscure. Therefore, we investigated the impact of maternal AA content on the growth of fetal mice during the gestation period using senescence marker protein-30/gluconolactonase (SMP30/GNL) knockout (KO) mice, which cannot synthesize AA in vivo.


SMP30/GNL KO mice gave birth after a gestation period under conditions of absent, low, or normal AA intake. AA was measured using high-performance liquid chromatography and electrochemical detection. Whole-body sections were stained with hematoxylin and eosin, Elastica van Gieson, and Azan.


The mothers in the group absent AA intake failed to bear young because of incomplete fetal development. Offspring born under the low-AA condition generally died within a few days after birth. Morphological analysis revealed that the latter neonates of SMP30/GNL KO mothers whose intake of AA was low during gestation manifested abnormal cardiac dilation, congestion of the liver and lungs, incompletely expanded pulmonary alveoli, and impaired vertebral bodies. In contrast, a normal AA diet produced healthy progeny.


A diet sufficiently replete with AA is essential during the gestational period for normal tissue development in the fetus and neonate.

[Indexed for MEDLINE]

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