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BOR - Papers in Press, published online ahead of print November 17, 2004.
Biol Reprod 2004, 10.1095/biolreprod.104.035238
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Submitted August 13, 2004
Returned for revision September 9, 2004
Accepted November 10, 2004

Testis


Infertility in 5,10-Methylenetetrahydrofolate Reductase (MTHFR)-Deficient Male Mice is Partially Alleviated by Lifetime Dietary Betaine Supplementation

Tamara L.J. Kelly , Oana R. Neaga , Bernd C. Schwahn , Rima Rozen , and Jacquetta M. Trasler *

* To whom correspondence should be addressed. E-mail: jacquetta.trasler{at}mcgill.ca.

Abstract
Metabolism of folate is essential for proper cellular function. Within the folate pathway, methylenetetrahydrofolate reductase (MTHFR) reduces 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a methyl donor for remethylation of homocysteine to methionine, the precursor of S-adenosylmethionine. S-adenosylmethionine is the methyl donor for numerous cellular reactions. In adult male mice, MTHFR levels are highest in the testis; this finding, in conjunction with recent clinical evidence, suggest an important role for MTHFR in spermatogenesis. Indeed, we show here that severe MTHFR deficiency in male mice results in abnormal spermatogenesis and infertility. Maternal oral administration of betaine, an alternative methyl donor, throughout pregnancy and nursing, resulted in improved testicular histology in Mthfr-/- offspring at postnatal day 6, but not at 8 months of age. However, when betaine supplementation was maintained post-weaning, testicular histology improved and sperm numbers and fertility increased significantly. We postulate that the adverse effects of MTHFR deficiency on spermatogenesis, may, in part, be mediated by alterations in the transmethylation pathway and suggest that betaine supplementation may provide a means to bypass MTHFR deficiency and its adverse effects on spermatogenesis by maintaining normal methylation levels within male germ cells.

Key words: Testis • Fertilization • Gametogenesis • Sperm • Spermatogenesis


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