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Vitamin C Deficiency Causes Hematological and Skeletal Abnormalities during Fetal Development in Swine^1,2,3,

Department of Anatomy and Physiology, Section for Veterinary Physiology and Biochemistry, Royal Veterinary and Agricultural University, DK-1870 Frederiksberg C, Denmark

The influence of maternal vitamin C deficiency on fetal development was studied in swine with a hereditary lack of ability to synthesize ascorbic acid (OD pigs). Thirteen pregnant sows homozygous (od/od) for the defect were depleted of ascorbic acid for 24 to 38 d at various stages of gestation. Six normal (OD/OD) sows were used as controls. Only a few experimental sows showed clinical symptoms of vitamin C deficiency. Nevertheless, severe pathological changes were seen in the uterus and fetuses. Characteristic findings were hemorrhages and hematomas in both fetal and maternal placenta, and general edema and subcutaneous hemorrhages in the fetuses. Similarities were noted to the abruptio placentae syndrome in women. Depletion of vitamin C resulted in a pronounced decline in ascorbic acid concentration in most maternal and fetal organs as well as in plasma and embryonic fluids. No morphological malformations were found in the fetuses, but the ossification of the skeleton was severely deranged. Macroscopically the lesions comprised swelling of the costochondral junction and separation of the epiphysial cartilage from the spongiosa in ribs and limb bones. Another characteristic finding was loosening of the periost from the cortex, often resulting in subperiosteal bleedings. Microscopically normal osteoblasts were few and the formation of osteoid defective.

KEY WORDS: • ascorbic acid deficiency • pigs • placental hemorrhages • ossification • fetal development

¹ Presented in part at the Second International Symposium on Ascorbic Acid in Domestic Animals, October 1990, Kartause Ittingen, Switzerland [Palludan, B. & Wegger, I. (1992) Ascorbic acid and fetal development in swine. In: Ascorbic Acid in Domestic Animals (Wenk, C., Fenster, R. & Völker, L., eds.), pp. 17–27. ETH Zentrum, Zürich, Switzerland].

² Supported by grants from the Danish Agricultural and Veterinary Research Council and Leo Research Foundation. The ascorbic acid used was a gift from Roche Denmark A/S.

³ The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

⁴ To whom correspondence should be addressed.

Manuscript received 17 June 1993. Revision accepted 22 September 1993.