期刊名称：Journal of Nutritional Science and Vitaminology
印刷版ISSN：0301-4800
电子版ISSN：1881-7742
出版年度：2016
卷号：62
期号：6
页码：375-379
DOI：10.3177/jnsv.62.375
出版社：Center for Academic Publications Japan
摘要：Spindle defect and chromosome misalignment occuring in oocyte meiosis induce nondisjunction. Nondisjunction causes Down syndrome, also known as trisomy 21. Folic acid (FA) is an essential nutrient composition for fetal growth and development. It has been reported that FA nutritional status is associated with the risk of Down syndrome. However, to our knowledge, little is known about the effect of FA deficiency on abnormal oocytes (spindle defects, chromosome misalignments and immature oocyte) in vivo. In the present study, we investigate the effects of FA deficiency on oocyte meiosis in female mice. In order to induce FA deficiency in mice, female Crl:CD1 mice were fed a FA-free diet for 58 d. The diet also contained an antibiotic which has functions on limiting FA formation by intestinal microorganisms. The level of FA deficiency was determined by measuring the concentration of FA in the liver, hemocyte, uterus, ovary, and urine. FA concentrations in these samples from the FA-deficient group were 50-90% lower. Despite this, the frequency of abnormal oocytes was no different between the FA-deficient and control groups (20.0% vs 14.6%). According to the past research, FA transporter was strongly expressed in oocytes. Hence, it is possible that FA-free diets may not affect the concentration of oocyte FA in mice. To sum up these data, our study concluded that FA deficiency did not adversely affect oocyte meiosis.
