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Am J Physiol Endocrinol Metab (December 13, 2005). doi:10.1152/ajpendo.00339.2005
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Submitted on July 26, 2005
Accepted on December 12, 2005

Ascorbic Acid-Independent Synthesis of Collagen in Mice

Kelly K Parsons1, Nobuyo Maeda2, Mitsuo Yamauchi3, Albert J Banes4, and Beverly H Koller1*

1 Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
2 Department of Pathology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
3 Department of Periodontology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
4 Department of Orthopaedics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

* To whom correspondence should be addressed. E-mail: treawouns{at}aol.com.

The mouse has become the most important model organism for the study of human physiology and disease. However, until the recent generation of mice lacking the enzyme gulanolactone oxidase (Gulo), the final enzyme in the ascorbic acid biosynthesis pathway, examining the role of ascorbic acid in various biochemical processes using this model organism has not been possible. In the mouse, similar to most mammals but unlike humans who carry a mutant copy of this gene, Gulo produces ascorbic acid from glucose. We report here that while ascorbic acid is essential for survival, its absence does not lead to measurable changes in proline hydroxylation. Vitamin C deficiency had no significant effect on the hydroxylation of proline and collagen production during tumor growth or in angiogenesis associated with tumor or mammary gland growth. This suggests that factors other than ascorbic acid can support proline hydroxylation and collagen synthesis in vivo. Furthermore, the failure of Gulo -/- mice to thrive on a vitamin C-deficient diet therefore suggests that ascorbic acid plays a critical role in survival other than the maintenance of the vasculature.




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