| First Author | Tempfer C | Year | 2000 |
| Journal | Fertil Steril | Volume | 73 |
| Issue | 5 | Pages | 1025-31 |
| PubMed ID | 10785232 | Mgi Jnum | J:89703 |
| Mgi Id | MGI:3041077 | Doi | 10.1016/s0015-0282(00)00417-9 |
| Citation | Tempfer C, et al. (2000) Genetic contributions of the endothelial nitric oxide synthase gene to ovulation and menopause in a mouse model. Fertil Steril 73(5):1025-31 |
| abstractText | OBJECTIVE: To investigate the influence of the endothelial nitric oxide synthase gene (Nos3) on ovulatory capacity and reproductive senescence. DESIGN: Prospective, controlled study. SETTING: Academic research institution. SUBJECT(s): Laboratory mice with targeted mutagenesis of Nos3. INTERVENTION(s): Hyperstimulation protocol, oocyte culture, and ovarian histology using wild-type (Nos3(+/+); n = 20), heterozygous (Nos3(+/m); n = 39), and homozygous deficient (Nos3(m/m); n = 11) female mice; observation of reproductive outcomes. MAIN OUTCOME MEASURE(s): Number and survival of oocytes; onset of menarche and menopause. RESULT(s): The mean number of superovulated oocytes (18 +/- 36 vs. 41 +/- 4) and the 48-hour overall survival rate of embryos (65% vs. 81%) were significantly reduced for Nos3(m/m) female mice compared with Nos3(+/+) female mice. Nos3(m/m) females showed a significantly reduced number and size of antral follicles and corpora lutea compared with wild-type controls. Compared with Nos3(+/m) x Nos3(+/m) breedings, Nos3(m/m) x Nos3(m/m) breedings showed a higher female age at first litter (76.2 +/- 10.3 vs. 107.8 +/- 26.6 days), fewer litters (10.5 +/- 3.6 vs. 7. 8 +/- 4.2), and a lower female age at reproductive senescence (400.2 +/- 64.5 vs. 332.1 +/- 27.4 days), respectively. CONCLUSION(s): Our data suggest that Nos3 deficiency is associated with reduced ovulatory capacity and impaired early embryonic viability and that it influences the onset of menarche and menopause. |
