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Development and characterization of ...
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Saint-Phar, Shawna.
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Development and characterization of a mouse model to determine the impact of low dietary folate on spermatogenesis, fertility and histone methylation.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Development and characterization of a mouse model to determine the impact of low dietary folate on spermatogenesis, fertility and histone methylation./
作者:
Saint-Phar, Shawna.
面頁冊數:
127 p.
附註:
Source: Masters Abstracts International, Volume: 48-02, page: 1035.
Contained By:
Masters Abstracts International48-02.
標題:
Health Sciences, Toxicology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=MR53607
ISBN:
9780494536070
Development and characterization of a mouse model to determine the impact of low dietary folate on spermatogenesis, fertility and histone methylation.
Saint-Phar, Shawna.
Development and characterization of a mouse model to determine the impact of low dietary folate on spermatogenesis, fertility and histone methylation.
- 127 p.
Source: Masters Abstracts International, Volume: 48-02, page: 1035.
Thesis (M.Sc.)--McGill University (Canada), 2009.
Folate is a critical determinant in male reproductive health. During spermatogenesis, there are massive alterations to the epigenome associated with tightly regulated gene transcription and chromatin reorganization including a tightly regulated pattern of histone H3 methylation. In vitro experiments were conducted to determine whether folate depletion could alter global histone H3 methylation at lysine 4 and 9 in cultured spermatogonia-like GC-1 cells. Folate depleted media did not alter global levels of histone H3 methylation at lysine 4 and 9 in spermatogonia-like GC-1 cell. In vivo experiments were used to determine the extent to which folate deficiency, from early embryonic development to adulthood, impacts histone methylation and male reproductive health in a mouse model. C57BL/6 females were fed either a folate-sufficient diet or a folate-deficient diet two weeks prior to breeding and through pregnancy and lactation. Male offspring received the same diet as their mother until sacrifice. Testes and epididymides were collected at postnatal day 6 to 18, and at 6 and 13--14 weeks of age. At 8 weeks of age, male pups were assessed in fertility trials. Folate deficiency severely compromised male reproductive health. Folate deficient males had reduced epididymis weight and defects in spermatogenesis. Abnormalities included the presence of multinucleated cells, sloughing of germ cells, and a slight increase in germ cell apoptosis. Alterations in key fertility parameters included an increase in sperm morphological defects and consequently decreased pregnancy rate and litter size. Remarkably, gene activating histone H3 tri-methylation at lysine 4 was significantly reduced in folate deficient males testes. This study is the first to assess the impact of folate deficiency on spermatogenesis, fertility and global histone methylation. The results strongly support a need for adequate folate intake to maintain male reproductive health and to ensure correct epigenetic programming during spermatogenesis.
ISBN: 9780494536070Subjects--Topical Terms:
1017752
Health Sciences, Toxicology.
Development and characterization of a mouse model to determine the impact of low dietary folate on spermatogenesis, fertility and histone methylation.
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Folate is a critical determinant in male reproductive health. During spermatogenesis, there are massive alterations to the epigenome associated with tightly regulated gene transcription and chromatin reorganization including a tightly regulated pattern of histone H3 methylation. In vitro experiments were conducted to determine whether folate depletion could alter global histone H3 methylation at lysine 4 and 9 in cultured spermatogonia-like GC-1 cells. Folate depleted media did not alter global levels of histone H3 methylation at lysine 4 and 9 in spermatogonia-like GC-1 cell. In vivo experiments were used to determine the extent to which folate deficiency, from early embryonic development to adulthood, impacts histone methylation and male reproductive health in a mouse model. C57BL/6 females were fed either a folate-sufficient diet or a folate-deficient diet two weeks prior to breeding and through pregnancy and lactation. Male offspring received the same diet as their mother until sacrifice. Testes and epididymides were collected at postnatal day 6 to 18, and at 6 and 13--14 weeks of age. At 8 weeks of age, male pups were assessed in fertility trials. Folate deficiency severely compromised male reproductive health. Folate deficient males had reduced epididymis weight and defects in spermatogenesis. Abnormalities included the presence of multinucleated cells, sloughing of germ cells, and a slight increase in germ cell apoptosis. Alterations in key fertility parameters included an increase in sperm morphological defects and consequently decreased pregnancy rate and litter size. Remarkably, gene activating histone H3 tri-methylation at lysine 4 was significantly reduced in folate deficient males testes. This study is the first to assess the impact of folate deficiency on spermatogenesis, fertility and global histone methylation. The results strongly support a need for adequate folate intake to maintain male reproductive health and to ensure correct epigenetic programming during spermatogenesis.
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