The Pharmaceutical Journal
Vol 268 No 7196 p597-604
4 May 2002

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Vitamin C transporter deficiency leads to death in newborn mice

Mice lacking the vitamin C transporter SVCT2 die within minutes of birth, American researchers have found. This may have important implications for human health, they say.

Dr Sotiria Sotiriou, National Human Genome Research Institute, Maryland, and colleagues found that SVCT2 is required for the prenatal transport of ascorbic acid into most tissues, particularly in the central nervous system and adrenal glands, and across the placenta. A lack of the transporter, and hence vitamin C levels and uptake, results in malformed lungs leading to respiratory failure and extensive bleeding in the brain in newborn mice, immediately after birth.

The researchers say that the study reveals a previously unrecognised requirement for ascorbic acid in the perinatal period and that "prenatal ascorbic acid deficiency deserves a more thorough investigation for its role, if any, in the morbidity due to premature birth" (Nature Medicine 2002; 8:514).

In an accompanying news and views article, Dr Matthias Hediger, Harvard Medical School, Boston, comments that the intracerebral haemorrhage observed in SVCT1-null mice "supports the notion that vitamin C and SVCT2 protect the brain from free radical damage".

Dr Hediger adds that it is also possible that "toxic accumulation of free radicals underlies the lung defect. Alternatively, collagen biosynthesis in the developing lungs may depend more on vitamin C than it does in other tissues" (ibid, p445).