Analysis Tools
reproductive system
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• TUNEL analysis revealed increased granulosa cell apoptosis at 4 weeks of age
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• primary ovarian follicles are depleted at 8 weeks of age, with only a few MVH-positive primary follicles found scattered in the cortical region
• however, number of primary follicles per ovary is normal at 3, 4 and 6 weeks of age
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• number of primordial ovarian follicles per ovary is markedly reduced at 3, 4 and 6 weeks of age
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• primordial ovarian follicles become depleted by 8 weeks of age, with only a few MVH-positive primordial follicles found scattered in the cortical region
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• number of secondary follicles per ovary is markedly reduced at 6 weeks of age
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• secondary ovarian follicles become depleted by 8 weeks of age
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• number of antral follicles per ovary is markedly reduced at 6 weeks of age
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• antral ovarian follicles become depleted by 8 weeks of age
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• although only a few follicles undergo atresia at 3 weeks, most follicles show signs of atresia by 4 weeks of age
• massive atretic follicles are noted at 6 weeks of age (sexual maturity): oocytes in atretic follicles are eliminated and the space is filled with granulosa cells
• nearly all types of follicles become depleted and no follicular structures are discernible in the ovaries by 8 weeks of age
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• ovary weight to body weight ratio is significantly decreased at 4, 6, and 8 weeks of age
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• ovary size is only slightly smaller at 3 weeks but sharply decreased from 4 to 8 weeks of age
• by 8 weeks, ovary size is reduced to about one fourth of that in control mice, indicating ovarian atrophy
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• female infertility is attributed to premature ovarian failure caused by massive follicle atresia
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• 6-8-week-old female mice fail to produce offspring during a 6-month mating period with wild-type males of known fertility
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cellular
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• TUNEL analysis revealed increased granulosa cell apoptosis at 4 weeks of age
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• at 2 weeks of age, small oocytes exhibit enhanced gammaH2AX signals indicative of accumulated unrepaired DSBs
• by 4 weeks of age, the DNA damage response pathway is elevated, as indicated by upregulation of phosphorylated p53 (S15) in the ovaries
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mortality/aging
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• female infertility is attributed to premature ovarian failure caused by massive follicle atresia
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endocrine/exocrine glands
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• TUNEL analysis revealed increased granulosa cell apoptosis at 4 weeks of age
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• primary ovarian follicles are depleted at 8 weeks of age, with only a few MVH-positive primary follicles found scattered in the cortical region
• however, number of primary follicles per ovary is normal at 3, 4 and 6 weeks of age
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• number of primordial ovarian follicles per ovary is markedly reduced at 3, 4 and 6 weeks of age
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• primordial ovarian follicles become depleted by 8 weeks of age, with only a few MVH-positive primordial follicles found scattered in the cortical region
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• number of secondary follicles per ovary is markedly reduced at 6 weeks of age
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• secondary ovarian follicles become depleted by 8 weeks of age
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• number of antral follicles per ovary is markedly reduced at 6 weeks of age
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• antral ovarian follicles become depleted by 8 weeks of age
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• although only a few follicles undergo atresia at 3 weeks, most follicles show signs of atresia by 4 weeks of age
• massive atretic follicles are noted at 6 weeks of age (sexual maturity): oocytes in atretic follicles are eliminated and the space is filled with granulosa cells
• nearly all types of follicles become depleted and no follicular structures are discernible in the ovaries by 8 weeks of age
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• ovary weight to body weight ratio is significantly decreased at 4, 6, and 8 weeks of age
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• ovary size is only slightly smaller at 3 weeks but sharply decreased from 4 to 8 weeks of age
• by 8 weeks, ovary size is reduced to about one fourth of that in control mice, indicating ovarian atrophy
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• female infertility is attributed to premature ovarian failure caused by massive follicle atresia
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homeostasis/metabolism
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• at 2 weeks of age, small oocytes exhibit enhanced gammaH2AX signals indicative of accumulated unrepaired DSBs
• by 4 weeks of age, the DNA damage response pathway is elevated, as indicated by upregulation of phosphorylated p53 (S15) in the ovaries
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